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79 54 blood pressure: Low Blood Pressure | Hypotension

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Blood Pressure Chart: Low, Normal, High Reading by Age

Published: 2017-11-19 – Updated: 2021-07-09
Author: Disabled World | Contact: Disabled World (Disabled-World.com)

Synopsis: Blood pressure chart reveals if adults and children have high, low, or healthy average blood pressure range for their age. Systolic Pressure is the blood pressure reading when your heart beats. This reading is always the the first or top number. Diastolic Pressure is blood pressure measurement when your heart relaxes. This is always the the second or bottom number.

Main Digest

NOTE: High blood pressure often does not cause any signs of illness that you can see or feel. Which is why it is important to make an appointment with your doctor – or other healthcare provider – to check your blood pressure.

What Does Blood Pressure Refer To?

Blood pressure refers to the force exerted by circulating blood on the walls of blood vessels and constitutes one of the bodies principal vital signs. The pressure of the circulating blood decreases as blood moves through your arteries, arterioles, capillaries, and veins. The term blood pressure generally refers to your arterial pressure, i.e., the pressure in the larger arteries, arteries being the blood vessels which take blood away from the heart.

Blood pressure is always given as two numbers;

  • Systolic Pressure (when the heart beats)
  • Diastolic Pressure (when the heart relaxes)

When the measurements are written, both are written as one above, or before, the other with the systolic being the first number, for example 120/75 (120 over 75).

Blood pressure measurement is NOT the same as your heart rate (pulse) or maximum heart rate measurement. Check what your heart rate for your age should be. You can calculate your predicted maximum heart rate by using the calculation: 220 – (age) = Age Predicted Maximum Heart Rate – or see our Target Heart Rate Calculator and Chart.

Measuring Your Blood Pressure

Healthcare professionals use a stethoscope and a manual sphygmomanometer to measure your blood pressure. Typically they take the reading above your elbow. The sphygmomanometer has a bladder, cuff, bulb, and a gauge. When the bulb is pumped it inflates the bladder inside the cuff, which is wrapped around your arm. This inflation will stop the blood flow in your arteries.

The stethoscope is used to listen for sound of the heartbeat, and no sound indicates that there is no flow. As the pressure is released from the bladder, you will hear the sound of the blood flowing again. That point becomes your blood pressure systolic reading. The diastolic reading is when you hear no sound again, which means that the blood flow is back to normal.

Low Blood Pressure Chart
What is Classed as LOW Blood Pressure?
Blood pressure that is too low is known as Hypotension.
Systolic pressure (mm Hg) Diastolic pressure (mm Hg) Pressure Range
90 60 Borderline Low blood Pressure
60 40 Too Low Blood Pressure
50 33 Dangerously Low Blood Pressure
Normal Blood Pressure Chart
What is Classed as NORMAL Blood Pressure?
Systolic pressure (mm Hg) Diastolic pressure (mm Hg) Pressure Range
130 85 High Normal Blood Pressure
120 80 Normal Blood Pressure
110 75 Low Normal Blood Pressure
High Blood Pressure Chart
What is Classed as HIGH Blood Pressure?
If one or both numbers are usually high, you have high blood pressure (Hypertension).
Systolic pressure (mm Hg) Diastolic pressure (mm Hg) Stages of High Blood Pressure
210 120 Stage 4
180 110 Stage 3
160 100 Stage 2
140 90 Stage 1

What Should Blood Pressure be According to Age?

Ideal Blood Pressure According to Age Chart
Age Female Male
1 – 2 80/34 – 120/75 83/38 – 117/76
3 100/59 100/61
4 102/62 101/64
5 104/65 103/66
6 105/68 104/68
7 106/70 106/69
8 107/71 108/71
9 109/72 110/72
10 111/73 112/73
11 113/74 114/74
12 115/74 116/75
13 117/75 117/76
14 120/75 119/77
15 120/76 120/78
16 120/78 120/78
17 120/80 120/78
18 120/80 120/80
19-24 120/79 120/79
25-29 120/80 121/80
30-35 122/81 123/82
36-39 123/82 124/83
40-45 124/83 125/83
46-49 126/84 127/84
50-55 129/85 128/85
56-59 130/86 131/87
60+ 134/84 135/88

NOTE: It is recommended that you get your blood pressure checked at least once every year by a healthcare provider. If you have been diagnosed with high blood pressure (or other related conditions), your doctor may recommend that you get it checked more often.

Printable Average Blood Pressure Reading Chart

Printable Average Blood Pressure Reading Chart.

Printable Blood Pressure By Age Chart

Printable Blood Pressure By Age Chart.

Who We Are:

Disabled World is an independent disability community established in 2004 to provide disability news and information to people with disabilities, seniors, and their family and/or carers. See our homepage for informative reviews, exclusive stories and how-tos. You can connect with us on social media such as Twitter and Facebook or learn more about Disabled World on our about us page.

Disclaimer: Disabled World provides general information only. Materials presented are in no way meant to be a substitute for professional medical care by a qualified practitioner, nor should they be construed as such. Any 3rd party offering or advertising on disabled-world.com does not constitute endorsement by Disabled World.


Cite This Page (APA): Disabled World. (2017, November 19). Blood Pressure Chart: Low, Normal, High Reading by Age. Disabled World. Retrieved August 13, 2021 from www.disabled-world.com/calculators-charts/bloodpressurechart.php

Treatment of systolic hypertension: spotlight on recent studies with angiotensin II antagonists

Since AII is believed to participate in the process of vascular remodelling and development of endothelial dysfunction frequently observed in hypertension patients, AIIAs may be especially useful in treating systolic hypertension. Activation of the renin–angiotensin system and sympathetic nervous system play a key role in mediating the haemodynamic changes that bring about systolic hypertension (ie, increased peripheral resistance, reduced arterial compliance, increased reflected waves and sodium retention).19 AIIAs may thus interfere with key mechanisms involved in the pathogenesis of ISH. They are also well tolerated, thereby potentially impacting the ability of hypertensive patients to stay on therapy and achieve goal SBP.

Overview of AII antagonist treatment trials in systolic hypertension

Losartan

The effects of losartan on SBP in patients with ISH have been reported in several placebo and active comparator trials.50, 51, 52 In a first prospective, placebo-controlled trial of an AIIA in ISH, Cushman et al50 compared the antihypertensive efficacy and tolerability of a losartan-based regimen and placebo in 308 patients with ISH. At 12 weeks, the placebo-adjusted mean change from baseline in trough sitting SBP was −11.6 mmHg, a value comparable to placebo-adjusted reductions seen in SHEP and Syst-Eur trials.15, 16

A double-blind, randomized, multi-country study by Farsang et al51 compared the efficacy and tolerability of losartan and atenolol after 16 weeks of treatment in 273 patients with a sitting SBP of 160–205 mmHg, and a sitting DBP < 90 mmHg. Patients whose SBP was not controlled were given additional treatment of HCTZ. While similar significant reductions in sitting SBP occurred in the losartan and atenolol groups, patients receiving losartan had a lower withdrawal rate due to clinical adverse events (1.5 vs 7.2%, P=0.035) and significantly fewer drug-related clinical adverse events (10.4 vs 20.3, P=0.029).

Similar findings were also reported in a study by Volpe et al,52 who compared a losartan-based and an amlodipine-based regimen on trough sitting SBP in a multicenter, prospective, randomized, double-blind, parallel-group study. Losartan and amlodipine produced comparable clinically relevant reductions in SiSBP; although losartan produced fewer clinical adverse events (67.8 vs 79.8%, P⩽0.001) and discontinuations (6.0 vs 14.6%, P⩽0.001) compared with amlodipine.

Eprosartan

This AIIA has been shown to lower blood pressure effectively in hypertensive patients over the recommended dose range of 600–800 mg once daily. 53 In patients with severe hypertension, eprosartan may be more effective than enalapril in reducing SBP.54 The blood pressure lowering effect of eprosartan appeared to be similar to that of enalapril with respect to DBP (mean change from baseline −20.1 vs −16.2 mmHg, respectively), but superior to enalapril with respect to SBP (mean change from baseline −29.1 vs −21.2 mmHg, respectively, P=0.025). However, in elderly patients with predominantly systolic hypertension, eprosartan and enalapril were equally effective in reducing sitting SBP and DBP.55

Valsartan

The effects of valsartan on SBP have also been evaluated in several placebo-controlled and active-control trials. In a study by Neutel et al,56 146 elderly patients with systolic hypertension, with or without diastolic hypertension, received valsartan 80 mg or placebo once daily for 4 weeks and were then force-titrated to valsartan 160 mg or matching placebo once daily for an additional 4 weeks. The reduction in trough sitting SBP with valsartan was superior to placebo (19.2 vs 8.8 mmHg, respectively, P<0.001). Valsartan also produced superior reductions in trough mean sitting DBP compared with placebo (5.2 vs 1.2 mmHg, respectively, P<0.001). Tolerability was comparable to that seen with placebo.

Malacco et al57 reported the blood pressure lowering effects of valsartan and amlodipine in elderly patients with ISH in Italy. In this 24-week, randomized, double-blind, active-controlled study, valsartan given alone or in combination with HCTZ showed similar efficacy but better tolerability than amlodipine-based treatment. Adverse events occurred in 31.9% of those receiving amlodipine vs 20.2% of the patients receiving valsartan (P< 0.003).

Candesartan

A number of studies have investigated the effects of candesartan on SBP. The efficacy and safety of candesartan and HCTZ (alone and in combination) was studied in a double-blind, randomized, placebo-controlled study in older patients with systolic hypertension. 58 Candesartan and low-dose HCTZ hydrochlorothiazide were effective and well-tolerated antihypertensive agents in ISH and produced additive effects when administered together. Both drugs were well tolerated either as monotherapy or in combination.

A study by Neutel et al59 in patients with ISH found that candesartan produced a dose-related decrease in SBP, with a smaller decrease in DBP, resulting in a substantial reduction in pulse pressure. The candesartan dose-blood pressure response was consistent across age, sex, and race. Adverse events were infrequent and led to withdrawal in only 8% of patients.

According to a large-scale study, candesartan either alone or as add-on therapy was effective for the control of systolic or diastolic hypertension across a wide range of demographic groups.60 This study involved a total of 6465 hypertensive patients, of which 1014 patients were diagnosed with ISH. Patients had either untreated or uncontrolled hypertension despite treatment with a variety of antihypertensive agents. In the cohort of patients with ISH, candesartan monotherapy reduced SBP/DBP by 17.0/4.4 mmHg. As add-on therapy, candesartan reduced SBP/DBP further by 17.4/5.1 mmHg in patients receiving diuretics, 15.6/3.6 mmHg in those receiving calcium antagonists, by 14.0/4.8 mmHg in those receiving beta blockers, and by 13.4/4.3 mmHg in those receiving ACE inhibitors. Candesartan was well tolerated with only 6.8% of the total cohort of 6465 patients withdrawing due to adverse events.

Telmisartan

In patients with mild to moderate hypertension, telmisartan at dosages of 40–160 mg daily significantly reduced SBP and DBP compared with placebo and was at least as effective as atenolol, amlodipine, or lisinopril.61, 62 In the AII receptor antagonist telmisartan in isolated systolic hypertension (ARAMIS) study, telmisartan (20–80 mg daily) produced significant reductions in SBP (16.9 mmHg at 80 mg dose) compared with placebo (11.4 mmHg) and produced reductions comparable to HCTZ 12. 5 mg (15.7 mmHg).63 As with other AIIAs, the tolerability of telmisartan was similar to that of placebo.

Irbesartan

Irbesartan produces 24-h blood pressure control in patients with mild-to-moderate hypertension and appears to be as effective as enalapril, atenolol, and amlodipine, and more effective than valsartan in terms of absolute reduction in BP and response rates.64 In a study of elderly patients aged 65 years or older with mild to moderate hypertension, irbesartan decreased mean sitting SBP by 10.1 mmHg, a value that was similar to that seen with enalapril (11.6 mmHg).65 As yet, no study has addressed the effects of irbesartan in patients with ISH. Irbesartan is well tolerated with an overall incidence of adverse events similar to that with placebo.64

Olmesartan

Olmesartan medoxomil (20–40 mg once daily), the latest addition to the ARB class, significantly reduces systolic and diastolic blood pressure in hypertensive patients of a magnitude comparable to that seen with amlodipine or other angiotensin receptor blockers, including losartan, valsartan, irbesartan. 66, 67, 68, 69 As yet, however, no studies have been reported in patients with ISH. Olmesartan appears to be well tolerated; only dizziness occurred with greater frequency with olmesartan medoxomil (3% of patients) than with placebo.67

Combination therapy

In a large proportion of patients with hypertension, combination therapy is essential to achieve BP control, especially with respect to SBP. This point is illustrated by the results of the HOT trial,70 which showed that normalization of SBP is usually only attained through administration of two or more agents. Indeed, several current hypertension guidelines (eg, Hypertension in African Americans Working Group (HAAWG) JNC7) and the latest European guidelines acknowledge that many patients with hypertension should receive a combination of two agents as initial therapy.9, 11, 71

Combination therapy using AIIAs and a low-dose thiazide diuretic such as HCTZ offers a number of potential benefits in antihypertensive therapy, including more effective blood pressure control and the likelihood of a better tolerability profile that can help patients stay on therapy. 72 The efficacy of losartan in combination with HCTZ in reducing SBP was recently compared with that seen with HCTZ monotherapies in patients with ambulatory systolic hypertension.73 Combinations of losartan 50 mg and HCTZ 12.5 mg and losartan 100 mg and HCTZ 25 mg provided greater reductions in clinic and ambulatory BP than HCTZ monotherapies. The enhanced antihypertensive efficacy of losartan–HCTZ combinations with respect to SBP may permit more rapid attainment of BP goals in a greater proportion of patients, thereby circumventing complex and tedious dose-titration schedules.

A recent meta-analysis also clearly showed that the combination of AIIA and HCTZ produces reductions in SBP that are markedly greater than those obtained with AIIA monotherapy.74 This analysis determined the antihypertensive efficacy of losartan, valsartan, irbesartan, and candesartan in a total of 43 published randomized controlled trials involving 11 281 patients. AIIA plus HCTZ combinations resulted in substantially greater reduction in systolic (16. 1–20.6 mmHg) and diastolic (9.9–13.6 mmHg) blood pressure reductions than AIIA alone and responder rates for AIIA/HCTZ combinations ranged from 56 to 70%.

Outcomes studies in systolic hypertension

LIFE The LIFE study compared losartan with beta-blocker atenolol, a conventional antihypertensive drug with documented CV benefits, on cardiac morbidity and mortality in hypertensive patients (aged 55–80 years) with signs of left ventricular hypertrophy (LVH).75, 76 A predefined subgroup of LIFE involved 1326 patients with LVH aged 55–80 years who also had ISH (SBP between 160 and 200 mmHg and DBP of <90 mmHg).76

The ISH substudy of LIFE demonstrated that losartan reduced the risk of combined CV morbidity and mortality, especially stroke and CV death, to a greater degree than atenolol for a comparable reduction in blood pressure (28/9 mmHg reduction in both arms). With respect to the primary end point, patients receiving losartan demonstrated fewer events than atenolol (25. 1 events vs 35.4 events per 1000 patient years, respectively, RR=0.75 after adjustment for risk and degree of LVH, P=0.059, Table 1). Compared with atenolol, losartan also decreased the risk of stroke (relative risk (RR)=0.60, P=0.02, Figure 3), CV mortality (RR=0.54, P=0.01), and new-onset diabetes (RR=0.62, P=0.04). However, losartan did not significantly affect the risk of MI (adjusted RR=1.12, P=0.41). Importantly, compared with atenolol treatment, losartan was associated with significantly lower discontinuation rate as a result of all serious adverse events (P<0.002) and drug-related adverse events (P<0.001).

Table 1 Effects of losartan and atenolol on end points in an ISH cohort of the LIFE studyFigure 3

Reduction in fatal and nonfatal stroke in ISH patients treated with losartan or atenolol in a predefined substudy of LIFE (data from Kjeldsen et al76).

The results of this substudy of LIFE demonstrate for the first time in patients with ISH that one antihypertensive treatment modality confers CV protective benefits over another proven antihypertensive therapy without clinically meaningful differences in blood pressure reduction. The greater CV benefits of losartan compared with atenolol most likely result from increased protection against the deleterious effects of AII but could also possibly be linked to unique molecule-specific effects of losartan (eg, attenuation of serum uric acid levels77 or other undefined mechanisms). The decrease in occurrence of new onset diabetes with losartan78 may be related to an interaction with the peroxisome proliferators-activated receptor-γ (PPARγ). Irbesartan, telmisartan, and, to a lesser degree, losartan have all been shown to induce PPARγ activity, a central regulator of insulin and glucose metabolism.79VALUE Results from the Valsartan Antihypertensive Long-term Use Evaluation (VALUE) study recently demonstrated BP control values better than those reported in most published large-scale trials. 80, 81 VALUE was designed to compare cardiovascular outcomes in 15 245 eligible hypertensive high-risk patients receiving valsartan or amlodipine-based treatment. The study showed that from 6 months to the end of the trial, both study groups produced decreases in BP (valsartan 3.3/2.6 mmHg and amlodipine 3.0/2.5 mmHg). Target SBP (<140 mmHg) was achieved in 58% of patients in the valsartan group and 64% of patients in the amlodipine group. No significant difference was observed between study groups for the primary composite end point of cardiac morbidity and mortality and for all-cause mortality. However, unequal control of BP in the valsartan and amlodipine groups makes it difficult to draw conclusions about the observed differences in some of the cause-specific outcomes.

The telmisartan Programme of Research tO show Telmisartan End-organ proteCTION (PROTECTION) programme82 comprises a number of trials to compare telmisartan with valsartan, losartan, amlodipine, and ramipril with respect to end-organ protective effects in patients at high risk of renal, cardiac, and vascular damage. The program includes studies on the effects of telmisartan in patients with ISH and is also expected to provide useful information on the value of AIIAs in hypertensive patient populations at high risk of clinical events.

7 Questions You’ve Always Had About Blood Pressure

 

1) What is blood pressure?

Blood pressure is the driving force in our body that keeps blood flowing to every organ. It is first generated by the powerful heart muscle and then maintained and transmitted by our blood vessels. Blood pressure has become synonymous with high blood pressure. For decades now, high blood pressure has been a well-recognized risk factor for heart attacks, strokes, and early death. High blood pressure is frequently referred to as the “silent killer” as no one knows what their blood pressure is, high or low, until they actually measure it. A majority of people will develop high blood pressure during their lifetime.

2) How do I know what my blood pressure is?

Figuring out what your blood pressure is, is easy. Any doctor appointment you go to will check your blood pressure. Health fairs, home blood pressure cuffs, even your neighbor who is a nurse can accurately measure your blood pressure.

3) What should my blood pressure be?

Over the years, goal blood pressure has been a moving target in terms of what your blood pressure should be, or more importantly what is should be under! Again every patient is different but as a general starting point, your systolic blood pressure (that’s the top number) should be less than 140 mmHg, and the diastolic blood pressure (that’s the bottom number) should be less than 90mmHg. If you are asking if one of those numbers is more important than the other, the answer is yes, it is the systolic (top) blood pressure that carries the most weight.

4) What can I do about it?

The first step to managing your blood pressure to change how you eat by greatly decreasing the amount of salt in your diet. In 2017, a vast majority of salt in a typical American diet comes from 2 places: 1) eating outside of the home. Whether it is a fast food meal or the finest 5-star restaurant, the food tastes good because it is loaded with salt and 2) you salt your food after it hits the plate before you eat it. By limiting eating outside of the home to two times a week or less and throwing away your salt shaker, you can help your blood pressure. Making dietary and lifestyle changes (exercise) you can on average lower your blood pressure by about 10 mmHg (i.e. 145mmHg -> 135mmHg).

RELATED: How to Control Your High Blood Pressure

5) So what about medication?

As you can see from the paragraph above, if your blood pressure is significantly elevated (>150/100 mmHg) it is very unlikely that diet and lifestyle changes alone will be enough to bring your blood pressure in a range that will reduce your risk or heart attacks, strokes, or early death. You need medications. The great thing about meds to treat your blood pressure is that there are A LOT of them. This means that you and your doctor should be able to find a regimen that works for you from a side effect standpoint.

6) What about cost?

A vast majority of blood pressure medications are generic and very affordable. In fact, if you are on an expensive brand medication for your blood pressure, ask your doctor about switching to a cheaper alternative that will be just as effective. You can also look at it in other ways, think of the cost to be admitted to the hospital with a heart attack with costly procedures or high risk surgeries. Spending pennies a day on your blood pressure pills may, in the future, save you tens of thousands of dollars.

7) When will I stop the medication?

More than likely you won’t. Very rarely does high blood pressure have a “cure.” A vast majority of people will need lifelong therapy for their blood pressure. Remember that heart disease is a disease of aging, and so being vigilant about controlling our risk factors (like high blood pressure) is a lifelong task.

Systematic Review and Meta-Analysis on Clinical Trial Studies

Background. Senescence refers to spontaneous and progressive irreversible degenerative changes in which both the physical and psychological power diminish significantly. Hypertension is the most common cardiovascular disease in the elderly. Several studies have been conducted regarding the effect of exercise on reducing the blood pressure of the elderly, which have found contradictory results. One of the uses of meta-analysis study is responding to these assumptions and resolving the discrepancies. Accordingly, the aim of the present study is to determine the impact of exercise on the blood pressure of older adults. Method. In this research, in order to find electronic published papers from 1992 to 2019, the papers published in both domestic and foreign databases including SID, MagIran, IranMedex, IranDox, Gogole Scholar, Cohrane, Embase, Science Direct, Scopus, PubMed, and Web of Science (ISI) were used. Heterogeneity index between the studies was determined based on Cochran test Q(c) and I2. Considering existence of heterogeneity, random effects model was employed to estimate the standardized subtraction of the mean exercise test score for reduction of blood pressure in the older adults across the intervention group before and after the test. Results. In this meta-analysis and systematic review, eventually 69 papers met the inclusion criteria. The total number of participants was 2272 in the pre- and postintervention groups when examining the systolic changes and 2252 subjects in the pre- and postintervention groups when inspecting the diastolic changes. The standardized mean difference in examining the systolic changes before the intervention was 137.1 ± 8.09 and 132.98 ± 0.96 after the intervention; when exploring the diastolic changes, the pre- and postintervention values were 80.3 ± 0.85 and 76.0 ± 6.56, respectively, where these differences were statistically significant (). Conclusion. The results of this study indicated that exercise leads to significant reduction in both systolic and diastolic blood pressure. Accordingly, regular exercise can be part of the treatment plan for hypertensive elderly.

1. Background

Senescence is a natural course of development in which special physical, psychological, and social changes occur [1]. In other words, senescence refers to spontaneous and irreversible progressive degenerative changes in which both psychological and physical power significantly decline [2]. In the elderly, all organs of the body undergo some degree of degeneration in all of their tasks; for this reason, various chronic diseases occur in the older adults including cardiovascular disease such as hypertension, coronary artery disease, and skeletal diseases such as arthritis, osteoporosis, and cancer [3].

Hypertension is the most common cardiovascular disease in the older adults [4], claiming high healthcare costs [4]. Since pharmacotherapy among the older adults necessitates adhering to various issues, today researchers tend to recommend nonpharmacological methods instead of pharmacotherapy considering the pathological mechanism of hypertension. Nonpharmacological methods include modifying the lifestyle through low sodium diet, low fat diet, increasing potassium as well as calcium intake, weight reduction in obese individuals, daily exercise, and reducing anxiety and fear [5]. Regular exercise at a moderate level for three days per week 30 min/day results in increased longevity, reduced mortality, and reduced development of cardiovascular disease, heart attack, hypertension, arthritis, osteoporosis, depression, and different types of cancer [6]. Regular aerobic exercise leads to reduction of both systolic and diastolic blood pressure by 11 and 8 mmHg. A regular physical activity program should start gradually and sustain for 30–45 min in most days of the week. This level of activity can control hypertension without pharmacotherapy [7].

The impact of aerobic exercises on hypertension has mostly been tested in long-term exercise programs (at least three months) with high intensity and high number of sessions per week (5 days/week). Increase in the number of exercise sessions per week and high intensity of exercise in individuals who are not able to do high intensity activities may be an obstacle to participating in such exercise programs [8]. There are different and sometimes contradictory responses to the numerous questions about the effect of different exercises and their varying intensities on the elderly’s blood pressure. Various research studies have reported different results about the impact of exercise on blood pressure considering the type of exercise, its conditions, duration, and frequency within a specific period, and its relationship with blood pressure reduction [9].

In the research by Moraes et al., after three days of aerobic exercise per week for three months in the intervention group, the mean systolic and diastolic blood pressure diminished by 3.2 and 1.2 mmHg, respectively, but no significant change was observed in the mean blood pressure of the control group [10]. In the research by Ferrier et al. , the arterial compliance showed resistance against a short aerobic exercise program, and no reduction was found in the blood pressure of patients [11]. The study by Tabara et al. with the aim of comparing aerobic short-term and long-term exercise programs with mild and moderate intensities on cardiovascular indicators of the older adults indicated that the short-term program had no impact on reducing systolic blood pressure, but it decreased the diastolic blood pressure. Long-term program resulted in diminished mean systolic and diastolic blood pressure from 136 to 129 and from 87 to 83, respectively. Also, both the mild and moderate intensity programs were influential for blood pressure reduction [12]. In the research by Westhoff et al., the impact of moderate intensity long-term exercise program was tested on patients with hypertension. The results showed blood pressure decline in the samples, though it was not statistically significant [13].

With regard to the impact of exercise on the blood pressure of the older adults with hypertension, some preliminary studies have been conducted across Asia, Europe, and America, which have found contradictory results. One of the uses of meta-analysis study is to address these assumptions and resolve the contradictions. Although Herrod et al. [14] conducted a meta-analysis study investigating the impact of exercise and other nonpharmacological measures on the blood pressure of the elderly, and this study has not tested the influence of exercise on the blood pressure of the older adults across different continents. Thus, the aim of this study is to determine the impact of exercise on the blood pressure of the older adults with hypertension across meta-analysis.

2. Methods
2.1. The Methods for Searching Papers

In this investigation, the search was performed on Persian databases including SID, MagIran, IranMedex, and IranDoc along with the international databases of Google Scholar, Cochrane, Embase, Science Direct, Scopus, PubMed, and Web of Science (ISI) with the aim of finding relevant papers without any time constraint (from 1992 to 2019). The list of the references utilized in all papers and the relevant reports found in the previously mentioned electronic search was assessed manually so that other possible references could also be found. The keywords used for searching the references were chosen from The Medical Subject Headings (MeSH) thesaurus. The keywords searched were exercise, resistance training, circuit-based exercise, plyometric exercise, exercise therapy, exercise training, physical activity, and hypertension (both in English and Persian).

((((((((((((Exercise[Title/Abstract]) OR Physical Activity[Title/Abstract]) OR Exercise Training[Title/Abstract]) AND Resistance Training[Title/Abstract]) OR Strength Training[Title/Abstract]) OR Weight-Bearing Exercise Program[Title/Abstract]) AND Circuit-Based Exercise[Title/Abstract]) OR Circuit Training[Title/Abstract]) AND Plyometric Exercise[Title/Abstract]) OR Plyometric Drill[Title/Abstract]) OR Plyometric Training[Title/Abstract]) OR Stretch-Shortening Cycle Exercise [Title/Abstract])))))))))))

2.2. The Criteria of Selection of Papers

The papers with the following characteristics were chosen for the meta-analysis: (1) original research papers, (2) clinical trials studies, and (3) availability of full text of papers. For the objectives of this investigation, physical exercise is any bodily activity that enhances or maintains physical fitness and overall health and wellness. It is performed for various reasons including strengthening muscles and the cardiovascular system, honing athletic skills, and weight loss or maintenance, as well as for the purpose of enjoyment [15]. The older adults were defined as individuals above 60 years of age, while hypertensive patients was defined as the patients with a medical diagnosis of hypertension for more than six months (it includes patients with a definite diagnosis of hypertension and does not include patients with prehypertension).

2.3. Exclusion Criteria

The selected studies were investigated more accurately. Those conducted as review or those whose sample had not been chosen from the older adults with hypertension or the studies repeated with previous data were removed from the meta-analysis. Eventually, 76 studies entered the third stage, qualitative assessment. Each article was separately reviewed by two reviewers. If the article was rejected by them, they expressed the reason, and if there was any controversy between the reviewers, the article was reviewed by a third referee whose opinion was considered as the final decision. Duplicate publication and multiple publications from the same population were removed using citation management software EndNote (version X7, for Windows, Thomson Reuters).

2.4. Qualitative Assessment of the Studies

The quality of the papers was evaluated based on the selected and relevant items of CONSORT checklist, which could be assessed in this study and already mentioned in previous studies (design of study, background and review of literature, place and time of the study, consequence, inclusion criteria, sample size, and statistical analysis). The papers mentioning six to seven criteria were considered of high quality, while those citing two or less of the seven mentioned items were considered as moderate and low quality papers in terms of their methodology [16]. In the present study, 69 papers were included in this systematic review and meta-analysis as being of high and moderate quality, while seven papers which were of low quality were excluded.

2.5. Data Extraction

All of the final papers introduced into the meta-analysis process were prepared for extraction by a premade checklist. The checklist included title of paper, name of the first author, year of publication, place of study, sample size of the intervention group, mean systolic and diastolic blood pressure before the intervention, mean systolic and diastolic blood pressure after the intervention, and standard deviation of systolic and diastolic blood pressure both before and after the intervention.

2.6. Statistical Analysis

Since the studied index was the impact of exercise on the blood pressure of the elderly, in order to combine the results of different studies, frequency and percentage were used along with standardized mean difference index in every study. In order to investigate homogeneity across studies, I2 index was used; considering the heterogeneity in the studies, random effects model was used to combine the studies and conduct the meta-analysis. Note that I2 < 25%, 25–75%, and greater than 75% represent low, medium [16], and high heterogeneity, respectively. was considered as statistically significant. Also, to investigate publication bias, funnel plot and Egger test were used.

3. Results

In this study, all studies conducted over the impact of exercise on the blood pressure of older adults were examined systematically without any time constraint and based on the PRISMA instructions. In the preliminary search, 1386 papers were identified; eventually, 69 studies published from 1992 to March 2019 were included in the final analysis (Figure 1).

The total number of participants was 2272 in the pre- and postintervention groups for investigating systolic changes, and 2252, for investigating diastolic changes. The characteristics of the studies included in this systematic review are shown in Table 1.


Author, year, and reference Place of study Sample size Mean ± SD of before SBP Mean ± SD of after SBP Mean ± SD of before DBP Mean ± SD of after DBP Quality

Haidari, 2014, [17] Iran 46 149.8 ± 4.63 144.9 ± 5.21 94.03 ± 3.66 85.9 ± 6.38 High
Amooali, 2015, [18] Iran 20 132.8 ± 13.66 121.9 ± 9.17 77.6 ± 7.89 74.9 ± 3.66 High
Hosseiny, 2007, [8] Iran 36 150.04 ± 12 149.5 ± 11 88.6 ± 6 84.6 ± 5 High
Tabara, 2007, [12] Japan 40 136 ± 19 129 ± 17 75 ± 11 70 ± 10 High
Noroalahi, 2019, [19] Iran 18 140. 33 ± 18.1 125.33 ± 15.1 83.94 ± 13.26 75.94 ± 11.33 High
Faramarzi, 2012, [20] Iran 20 131.13 ± 18.5 123.63 ± 11.1 86.48 ± 3.5 81.61 ± 1.8 High
Behjati Ardakani, 2018, [21] Iran 24 131.1 ± 18 123.5 ± 11.1 86.4 ± 3.45 81.6 ± 1.8 High
Ghasemian, 2013, [22] Iran 20 131.3 ± 10.5 121.63 ± 11 86.88 ± 3.5 80.1 ± 0.8 High
Kawasaki, 2011, [23] Japan 35 136.6 ± 3.2 127 ± 2.7 81 ± 1.6 77.5 ± 1.3 Medium
Yin, 1998, [24] Japan 25 137.0 ± 10 135 ± 14 80 ± 7 78 ± 8 Medium
Wong, 2019, [25] Korea 52 146 ± 8.1 135 ± 1 88 ± 1 79 ± 1 High
Ruangthai, 2019, [26] Thailand 13 141 ± 15. 9 128.3 ± 15.4 84.1 ± 10 76.6 ± 7.5 High
Hamdorf, 1999, [27] Australia 144.6 ± 4.9 139.8 ± 4.2 72.6 ± 2.2 74 ± 1.8 Medium
Lee, 2007, [28] Taiwan 102 152 ± 10.5 136.2 ± 16.7 83.5 ± 11.2 76.7 ± 12.3 High
Lim, 2015, [29] Korea 10 129.4 ± 12.7 124.5 ± 9.2 80.8 ± 6.7 78.1 ± 6.7 High
Miura, 2015, [30] Japan 45 150 ± 9.1 145 ± 8.9 83.5 ± 5.9 80.2 ± 6.2 High
Ohkubo, 2001, [31] Japan 121 134.2 ± 2.4 127.6 ± 2.3 79.1 ± 1.3 76.9 ± 1.3 High
Okumiya, 1996, [32] Japan 21 136.4 ± 22.6 140.9 ± 22.8 78.1 ± 11.8 73.6 ± 11.2 High
Patil, 2015, [33] India 30 146. 87 ± 5.72 154.83 ± 6.33 74.2 ± 4.6 75.57 ± 5.68 High
Sunami, 1999, [34] Japan 20 142 ± 22 140 ± 19 83 ± 11 81 ± 11 Medium
Thomas, 2005, [35] Hong Kong 64 142 ± 17 142 ± 23 72 ± 13 72 ± 14 Medium
Pitsavos, 2011, [36] Greece 52 131.5 ± 13.48 119.45 ± 6.87 83 ± 4.97 76.55 ± 4.88 High
Deiseroth, 2019, [37] Switzerland 25 132 ± 15 128 ± 16 88 ± 10 78 ± 8 High
del Pozo-Cruz, 2012, [38] España 21 140.55 ± 12.9 133.3 ± 20.26 86.1 ± 8.16 77.65 ± 6.64 High
Di Mauro, 1998, [39] Italy 35 156.1 ± 15.3 154.4 ± 13.6 97 ± 7.7 94.7 ± 6.5 Medium
Leibovitz, 2005, [40] Israel 25 131 ± 3 130 ± 2 73 ± 1 74 ± 1 High
Broman, 2006, [41] Sweden 15 138 ± 9 138 ± 14 79 ± 8 75 ± 7 High
Chomiuk, 2013, [42] Poland 44 134. 61 ± 13.1 129.67 ± 11.7 75.67 ± 8.46 73.22 ± 8.04 High
Dimeo, 2012, [43] Germany 24 138.4 ± 14.1 132.5 ± 10.8 78.3 ± 10.2 75 ± 9.8 High
Faulkner, 2013, [44] New Zealand 36 141 ± 16 136 ± 16 82 ± 9 80 ± 9 Medium
Finucane, 2010, [45] UK 50 138.8 ± 15 135.8 ± 12.5 76.8 ± 8.6 75.2 ± 9.1 High
Kallinen, 2002, [46] Finland 12 174 ± 15 164 ± 16 83 ± 3 80 ± 2 Medium
Niederseer, 2011, [47] Austria 22 123.1 ± 11.9 122.6 ± 13.4 82.4 ± 11.2 78.1 ± 9.5 High
Puggaard, 2000, [48] Denmark 22 153 ± 37 161 ± 31 77 ± 16 84 ± 22 High
Sousa, 2013, [49] Portugal 16 149. 4 ± 25.1 148.5 ± 15.1 80.4 ± 7.6 82.8 ± 9.6 High
Westhoff, 2008, [13] Germany 12 134 ± 20 127 ± 16.4 73 ± 21.6 67.1 ± 8.2 High
Peters, 2006, [50] USA 10 146 ± 11 133 ± 14 90 ± 7 88 ± 11 High
Ditor, 2005, [51] Canada 8 117 ± 20.3 114.8 ± 15 73.3 ± 10.6 71.8 ± 9.4 High
Cunha, 2011, [52] Brazil 30 134.41 ± 17.5 126.81 ± 16.1 81.65 ± 10.57 76.35 ± 10.28 High
Cunha, 2012, [53] Brazil 16 135.46 ± 7.42 126.93 ± 11.5 76.09 ± 6.49 72.84 ± 5.08 High
de Freitas Brito, 2014, [54] Brazil 10 147 ± 4 146 ± 3 93 ± 4 91 ± 3 Medium
Júnior, 2019, [55] Brazil 10 162. 5 ± 11.2 160 ± 9.1 90 ± 5.9 80 ± 7.6 High
Lowenthal, 2004, [56] USA 25 128 ± 3 126 ± 4 86 ± 4 78 ± 3 High
Moreira, 2016, [57] Brazil 23 125.2 ± 9.3 114.7 ± 5.3 72 ± 6.8 71 ± 5.7 High
Mota, 2013, [58] Brazil 32 134.5 ± 14.6 122.4 ± 13.8 80.9 ± 11.1 73.2 ± 9.5 High
Santana, 2011, [59] Brazil 10 129 ± 17 125 ± 14 77.0 ± 8 77 ± 7 High
Scher, 2010, [60] Brazil 16 130 ± 15 128 ± 10 80 ± 8 76 ± 8 High
Toth, 2006, [5] USA 50 148.3 ± 22.8 140.5 ± 27.2 Medium
Chan, 2018, [61] USA 82 142.39 ± 17. 3 138.15 ± 17.3 81.83 ± 11.65 79.74 ± 10.51 High
Costa, 2019, [62] Brazil 23 121.5 ± 11.2 119.2 ± 6.9 71.1 ± 8.4 70 ± 7.8 High
Nascimento, 2019, [63] Brazil 27 126.04 ± 11.04 118.08 ± 9.09 72.95 ± 6.47 69.02 ± 6.54 High
Kling, 2019, [64] USA 10 137.1 ± 22.3 124.7 ± 19.4 76.3 ± 12.2 76 ± 9.5 High
Leandro, 2019, [65] Brazil 24 142.96 ± 20.91 124.12 ± 9.95 79.48 ± 19.48 61.68 ± 11.07 High
Braith, 1994, [66] USA 19 120 ± 9 112 ± 11 75 ± 7 68 ± 6 Medium
Applegate, 1992, [67] USA 56 145 ± 10 143 ± 12 88 ± 4 87 ± 2 Medium
Barone, 2009, [68] USA 51 140 ± 8 134. 7 ± 10.1 77 ± 7 73.4 ± 4.8 High
Bouchonville, 2014, [69] USA 26 131.2 ± 11.7 130 ± 15.5 70.9 ± 8.3 68.8 ± 6.1 High
Dusek, 2008, [70] USA 61 146.3 ± 5.5 145.3 ± 4.7 77.3 ± 7.1 77.6 ± 7.8 High
Gerage, 2013, [71] Brazil 15 125 ± 8 120 ± 7 81 ± 6 80 ± 6 Medium
Goncalves, 2014, [72] Brazil 17 126 ± 5.2 122.9 ± 4.4 80.9 ± 3.3 81.9 ± 4.4 High
Jessup, 1998, [73] USA 11 134.7 ± 11.9 129.4 ± 11.5 76.9 ± 5.1 72.1 ± 7.4 High
Li, 2005, [74] USA 54 135.02 ± 13.51 125.98 ± 13.1 78.59 ± 11.06 72.83 ± 10.63 Medium
Madden, 2010, [75] Canada 20 143 ± 3 139 ± 4 85 ± 2 86 ± 2 High
Millar, 2008, [76] Canada 25 122 ± 2. 8 117 ± 2.8 70 ± 1.3 68 ± 1.6 High
Simons, 2006, [77] USA 64 133 ± 12 128 ± 9 68 ± 6 70 ± 4 Medium
Wang, 2011, [78] USA 180 131.9 ± 17.6 128.2 ± 17.8 68.7 ± 10.7 67.5 ± 9.4 High
Wood, 2001, [79] USA 11 153.3 ± 10.8 146.6 ± 15.6 81.3 ± 7.2 70.9 ± 8.2 High
Yassine, 2009, [80] USA 24 135.6 ± 11.2 121.1 ± 11.2 81.6 ± 11.2 71.6 ± 9.6 High
Mortimer, 2011, [81] South Africa 15 130.6 ± 6.4 123 ± 9.1 83.88 ± 4.1 78 ± 5.1 High

Based on the available data, for final estimation of the effects of studies, standardized mean difference indices were used in the papers. In the studies that had reported standard deviation ± mean, standardized mean difference index was used in the meta-analysis. The results obtained from meta-analysis showed that across the studies, heterogeneity in investigating systolic changes pre- and postintervention was obtained as I2 = 98.8 and 98.6, while it was 99.2 and 98.6, respectively, for diastolic changes. Thus, for combination of studies and the final results, random method was used.

In order to investigate publication bias in the studies, Egger test was used. According to the results of this test, publication bias did not exist in investigating systolic changes pre- () and postintervention () and investigation of diastolic changes before () and after the intervention () (Figures 2–5).




Based on the results obtained from the meta-analysis, the standardized mean difference in examining the systolic changes pre- and postintervention was obtained as 137. 8 ± 1.09 and 132.08 ± 0.96, while, for diastolic changes, they were 80.3 ± 0.85 and 76.6 ± 0.56, respectively. All of these suggest that exercise leads to diminished hypertension during advanced ages. In the cumulative figures, the standardized mean difference index, confidence interval of 95% in each study, and the final result of the index obtained from combining the studies have been shown. In this diagram, the weight of each study has been shown in the final combined value, where the size of each square is in proportion with the weight that the study has had in the meta-analysis. The horizontal line of each square represents the confidence interval of 95% (Figures 6–9).




According to Table 2 reporting the mean and standard deviation of pre-/postintervention in systolic and diastolic blood pressure changes in terms of different continents (Asia, Europe, Africa, and America), 21, 15, 1, and 32 papers were analyzed in the meta-analysis from Asia, Europe, Africa, and America, respectively. In all of the investigations in terms of the studies carried out in the mentioned continents, exercise led to reduced age-induced hypertension (Figures 10 and 11).


Blood pressure changes Continents Number of articles I2 Sample size Egger test Mean ± SD

Systole (before intervention) Asia 21 99.2 806 0.706 140.4 ± 1.7
Europe 15 94.1 411 0.051 140.2 ± 2.4
America 32 98 1040 0.503 135.3 ± 1.8
Africa 1 0 15 130.6 ± 1.6

Systole (after intervention) Asia 21 99 806 0.627 134. 2 ± 1.8
Europe 15 96.1 411 0.119 136.5 ± 2.4
America 32 98.6 1040 0.793 129.1 ± 2.1
Africa 1 0 15 123 ± 2.3

Diastole (before intervention) Asia 21 99.5 806 0.990 81.8 ± 1.3
Europe 15 98 411 0.051 81.2 ± 2.01
America 31 98.6 990 0.138 78.7 ± 1.5
Africa 1 0 15 83.8 ± 1.05

Diastole (after intervention) Asia 21 97.7 806 0.797 78.1 ± 0.56
Europe 15 97 411 0.111 77.9 ± 1.4
America 31 99. 1 990 0.207 75.06 ± 1.6
Africa 1 0 15 78 ± 1.3


3.1. Standard Difference in Mean

In the study of the mean difference between systolic and diastolic blood pressure changes pre- and postintervention, it was reported that the difference between the systolic blood pressure changes pre- and postintervention was 0.65 ± 0.09, which showed a decrease in the systolic blood pressure after exercise (Figure 12), and the difference between the diastolic blood pressure changes pre- and postintervention was 0.64 ± 0.3609, which showed a decrease in the diastolic blood pressure after exercise (Figure 13).


3.2. Subgroup Analysis Based on the Type of Exercise

Subgroup analysis based on the standard difference in mean before and after the intervention according to the type of exercise shows that resistance exercises reduces systolic (0. 69 ± 0.1) and diastolic blood pressure (0.73 ± 0.16) more than aerobic exercise (Table 3).


Type of exercise Number of articles Sample size I2 Egger test Std. difference in mean (before and after intervention)

Aerobic exercise Systolic blood pressure 48 1734 94.4 0.715 0.69 ± 0.16
Diastolic blood pressure 89.5 0.178 0.64 ± 0.11

Resistance exercises Systolic blood pressure 20 494 54.6 0.051 0.69 ± 0.1
Diastolic blood pressure 82.8 0.053 0.73 ± 0.16

4.

Discussion

Hypertension is one of the most common diseases in industrial countries [82] and one of the important causes of atherosclerosis, which can cause different problems. In case the treatment is not received, 50% of patients with hypertension die because of coronary artery diseases and congestive heart failure, 33%, because of stroke, and 10–15%, due to renal complications. Further, other organs including the eyes and larger vessels can also be affected [83]. Thus, the aim of the present study is to determine the impact of exercise on the blood pressure of the older adults with hypertension across Asia, Europe, Africa, and America through meta-analysis.

Based on the results obtained from the meta-analysis here, the standardized mean difference in investigating the systolic changes before and after the intervention was 137.8 and 132.08, respectively, and, for diastolic changes, 80.3 and 76.6, respectively. All these suggest that exercise causes a significant decline in age-induced hypertension.

Chronic hypertension adversely affects the myocardial structure and function, inducing a concentric hypertrophy [84]. It seems that the hypertrophic cardiac response to the overpressure is an attempt for normalizing the ventricular walls, thus helping preserve the heart function when undergoing an increased hemodynamic load. This process of hypertrophy is called compensatory hypertrophy [85]. Physical exercise leads to proper adaptation in the cardiovascular system, thereby reducing heart rate, resting heart rate, and increased left ventricle filling, venous return, and stroke volume [86]. In a research by Hinderliter et al., they concluded that after a six-month aerobic exercise program, the left ventricle hypertrophy of patients with hypertension diminished significantly. This reduction of hypertrophy was associated with reduced blood pressure and weight loss of patients. These researchers also found that weight loss is an important factor in mitigating the left ventricle hypertrophy [87]. In addition, Kokkinos et al. observed that aerobic exercise can lead to diminished hypertrophy in hypertensive individuals [88]. Notwithstanding, following aerobic exercise, eccentric contractions occur, whereby the ventricle volume grows; hypertrophy in the ventricle is also possible to occur though to a little extent (in healthy subjects). However, when the subjects are hypertensive, since they have pathologic hypertrophy in the ventricle wall, the mechanism is different. This means that, upon physiological increase in the ventricle dimensions (resulting from aerobic activity) and according to Frank-Starling law, the stroke volume increases and thus pathologic hypertrophy of the ventricular wall diminishes [89].

The present study indicates the results of mean and standard deviation before and after the intervention in changes of systolic and diastolic blood pressure for different continents. These changes have been reported for Asia, Europe, Africa, and America. In all of the investigations conducted across different continents, it was reported that exercise leads to significant reduction of age-induced hypertension. The real mechanism of postactivity hypotension is unknown, and most probably the mechanism is multifactorial. Studies suggest that acute hypotension is mostly associated with diminished peripheral resistance of vessels rather than cardiac output [90]. According to animal and human studies, diminished sympathetic activity occurs after physical exercise [91–93]. Changes in reactivity of vessels are associated with reduced sympathetic conduction for vessel resistance and release of local vasodilator substances (e.g., nitric oxide) in response to muscle contraction and increased blood flow to the muscles. After a heavy physical exercise, reactivity of vessels to alpha-adrenergic stimulation diminishes [94]. The local release of nitric oxide, prostaglandins, and adenosine increases during physical activity, thus facilitating peripheral postactivity vasodilation [95].

Postexercise hypertension is a result of physical activity, and daily changes of blood pressure do not affect its reduction. The density and volume of physical exercise play an important role in hemodynamic and thermal regulation as well as regulation of neurological reactions of the body during activity [96]. Also, Syme et al. reported that the intensity of physical activity influences the duration of hypotension and has a direct relationship with it [97]. Studies show that possibly factors such as diminished plasma volume, increased vasodilation substances, changes in the hormones affecting blood pressure including vasopressin, angiotensin 2 and renin, and peripheral vasodilation resulting from elevated central temperature are effective in inducing hypotension [98].

Use of physical exercise in the long run functions as a no pharmacological method for blood pressure reduction at rest or during daily physical activities [99]. In the elderly, exercise may be a more suitable method for controlling blood pressure because of low cost and not interfering with other treatments. Through exercise and physical activity, the adverse physiological effects that occur with the aging can be mitigated and the quality of life can be improved [100]. One session of mild or moderate intensity exercise can lead to blood pressure fall after exercise in hypertensive individuals, which is called postexercise hypotension [101].

In the human, postexercise hypotension is observed in response to several types of exercise in which large muscles are active including jogging, cycling, running, and swimming [102].

Through exercise, the oxidation capacity of muscles increases, whereby the aerobic biochemical system is stimulated to create adaptation. All these result in enhanced oxygen uptake in the body. Some diseases cause inhibition of oxygen in any of the above stages and reduce the functional capacity. However, aerobic exercises are able to create physiological adaptation in the efficiency of the aerobic energy system. They also enhance the functional ability of the person and improve the functional capacity even under progression conditions of the disease. Other advantages of regular exercise in this group of patients include increased power, improved body posture, diminished fatigue, improved mood, increased self-confidence, and sense of well-being. Doing physical exercise increases the persons’ independence thereby leading to improved quality of life [103, 104].

Since these methods are easy to learn and possible to perform for almost all patients and there is no need to special equipment or cost, and even the patient can perform them in a lying position, patients can learn these methods easily and do them at home. By benefiting from the impacts of exercise methods such as greater blood perfusion to the muscles and reduction of stress and anxiety, their hypertension would diminish and their performance would be boosted. Also, through training patients on these methods and supervision on the way they should be practiced, the disturbing symptoms of this disease can be mitigated. Thus, by educating this method to both the healthcare team and patients, effective steps can be taken to alleviate this disorder.

It is recommended that relevant specialists benefit from regular aerobic exercise as a complementary treatment alongside pharmacotherapy to help patients with hypertension.

One of the limitations of the present research was completing the sheet of doing the exercise at home by the patients in the papers introduced to this meta-analysis, which may have been affected by the psychological status or inadequate care of the samples. Nevertheless, in some papers, checking whether exercise was done was followed up through a weekly in-person meeting with the patients.

5. Conclusion

The results of this study indicated that exercise significantly reduces blood pressure in the older adults across different continents. Accordingly, regular physical exercise can be part of the healthcare program of older adults with hypertension.

Abbreviations
SID: Scientific information database
CONSORT: Consolidated standards of reporting trials
PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-analysis.
Data Availability

Datasets are available from the corresponding author upon reasonable request.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Authors’ Contributions

MK and NR contributed to the design, and MM and RJ were responsible of statistical analysis and participated in most of the study steps. AVR and AD prepared the manuscript. NS and MM assisted in designing the study and helped in the interpretation of the study. All authors have read and approved the content of the manuscript.

Acknowledgments

This work was funded by the Student Research Committee of Kermanshah University of Medical Sciences Deputy for Research and Technology, Kermanshah University of Medical Sciences (IR) (3009270).

Connexin 43: a New Therapeutic Target Against Chronic Kidney Disease – FullText – Cellular Physiology and Biochemistry 2018, Vol. 49, No. 3

Abstract

Chronic kidney disease is an incurable to date pathology with a continuously growing incidence that contributes to the increase of the number of deaths worldwide. With currently no efficient prognostic or therapeutic options being available, the only possibility for treatment of end-stage renal disease is renal replacement therapy through dialysis or transplantation. Understanding the molecular mechanisms participating in the progression of renal diseases and uncovering the pathways implicated will permit the identification of novel and more efficient targets of therapy. Connexin43 was recently identified as a novel player in the development of chronic kidney disease. It was found de novo expressed and/or differentially localized in various renal cell populations during progression of renal disease, indicating an abnormal connexin signaling, both in patients and animal models. Subsequent in vivo studies demonstrated that connexin43 is involved in mediating inflammatory and fibrotic processes contributing to renal damage. Genetic, pharmaco-genetic or peptide-based inhibition of connexin43 in animal models and cell culture systems was successful in preventing the progression of the pathology and preserving the cell phenotypes. This review will summarize the recent advances on connexin43 in the field of kidney diseases and discuss the potential of future connexin43-based therapies against chronic kidney disease.

© 2018 The Author(s). Published by S. Karger AG, Basel


Introduction

Chronic kidney disease (CKD) is a major burden of public health associated with high morbidity and mortality worldwide. The number of patients suffering from CKD is constantly growing because of aging of the population, improved survival from cardiovascular diseases, and spreading of type-2 diabetes [1]. The most common causes of CKD include diabetes mellitus followed by high blood pressure and glomerulonephritis. The remaining cases can be due to polycystic kidney disease, obstructive nephropathy, pyelonephritis and others [2]. These pathologies may affect any of the kidney structures including renal vessels, glomeruli, and the tubulointerstitial compartment. Despite their different origin, renal diseases share common mechanisms involving inflammatory processes and the pathological accumulation of extracellular matrix which lead to gradual impairment of renal structure and function [3, 4]. Maintenance of normal renal parenchyma and homeostasis is essential for preservation of renal function and protection from CKD [3, 4]. Although our understanding of the mechanisms implicated in the development of renal diseases has been reinforced over the last years, there is a current lack of available early prognostic markers and therapeutic options against CKD, which necessitates the discovery of more targeted and efficient treatments [3, 4].

Connexins

Tissue homeostasis and structural integrity is maintained by specialized protein structures involving tight, adherens and gap junctions. Gap junctions are composed of two intercellular hemichannels, the connexons, which allow the direct communication between adjacent cells [5]. Connexons are localized on the plasma membrane of two neighboring cells and create a hydrophilic pore between the cytoplasm of the connected cells allowing the exchange of low molecular weight chemical mediators like ions (Ca2+, Na+, etc.) and second messenger molecules (cAMP, IP3, etc.) [6]. Apart from cell-to-cell communication, uncoupled connexons can exert the same functions as a complete gap junction, therefore allowing cell-to-matrix communication [7]. Connexons consist of six connexins forming a homo- or a heterohexamer. Connexins are named according to their predicted molecular weight; 20 connexin genes have been identified in mice and 21 in humans, sharing significant homology [8]. Besides specific exceptions like erythrocytes, thrombocytes mature skeletal muscle fibers and spermatozoids, gap junctions are present among all types of cells [9]. Gap junctions therefore provide a universal function as intercellular channels of communication that form the basis of direct cellular interactions. Given the relatively low specificity of gap junctions that allows passage of diverse molecules, it is not surprising that they are involved in a wide variety of physiological functions in different cell types including cell growth [10], glandular secretion [11], vascular homeostasis and angiogenesis [12], proliferation [13], bone development [14], cardiac morphogenesis [15, 16], glial function [17] and neuronal migration [18], stem cell development [19] and others.

Earlier studies have reported that several connexin isoforms are implicated in the renal physiopathology. Nearly half of the 20 members of the connexin family were found to be expressed throughout different renal compartments, at least at the mRNA level, including Cx26, Cx30.3, Cx31, Cx32, Cx37, Cx40, Cx43, Cx45, and Cx46 [20, 21]. However, connexin mRNA and protein expression do not always correlate and conflicting data regarding connexin expression and localisation have been reported. In this review we will mainly focus on the role of Cx43 in chronic renal disease.

Connexin43

Connexin43 (Cx43) is considered as the most widely expressed connexin. As is the case with other connexins, extensive studying of Cx43 has revealed that apart from its role in cell-to-cell communication, it can mediate gene transcription, cytoskeleton dynamics, ATP exocytosis, vesicle release and cell stress [22]. Cx43 is abundantly expressed in the heart and is indispensable for heart development and myocyte function [23]. Similarly, it is the most widely expressed connexin in the retina, but its role goes beyond cell communication since it can be part of a pathogenic pathway that leads to loss of retinal epithelium [24]. In contrast, vascular Cx43 has been shown to have a deleterious role in progression of atherosclerosis since reduction of its expression had a protective, possibly anti-inflammatory, effect in atherosclerosis susceptible mice [25]. In the brain, Cx43 is the main connexin in astrocytes but its exact role in neuronal physiology and neurodegeneration is disputed with contradicting evidence on whether it exerts a neuroprotective or deleterious role [26]. In osteoblasts and osteocytes, Cx43 hemichannels are considered necessary for cell survival [27] while it is central to spermatogenesis and testis homeostasis [28]. Finally, Cx43 is expressed in several tumor types including liver, prostate, and breast. Its role in carcinogenesis and metastasis is far from straight forward since it has been shown that Cx43 can have both pro- [29] and anti-metastatic capacity in different tumors [30] which indicates a tissue or even cell-specific way of action.

Connexin43 in the kidney

Cx43 was first detected in the rat kidney in 1989 [31]. Barajas et al. provided a more complete study and concluded that Cx43 localizes in renal vasculature, mesangial cells and collecting ducts [32]. In 1997, Hillis et al. studied Cx43 expression in biopsies from patients with different inflammatory glomerulopathies and found it strongly expressed by infiltrating cells and suffering tubular epithelial cells, as well as de novo expressed in interstitial sites of injury [33]. Broadening the spectrum of renal pathologies involving Cx43 upregulation, a Japanese group reported the presence of Cx43 in normal podocytes in a linear pattern and a shift in this linear distribution in patients with diabetic nephropathy, [34] while Guo et al. reported decreased Cx43 in glomeruli of diabetic patients without specifying the cell types implicated [35]. In vitro data from renal epithelial cells exposed to high glucose, provided for the first time a functional explanation for Cx43 upregulation under stressful conditions, indicating that Cx43 gap junctions mediate the emission of deleterious Ca+2 signals [36]; however the exact role of Cx43 in the progression of renal disease remained unclear. In parallel, many studies focused on a possible role for Cx43 on renin secretion and regulation of blood pressure. Initial reports suggested that Cx43 promoted renin secretion. The replacement of Cx43 by Cx32 in transgenic mice reduced the expression and secretion of renin and prevented the renin-dependent hypertension in the 2K1C (2-kidney, 1-clip) model [37]. However, Takenaka et al. demonstrated that a specific Cx43 blocking peptide (GAP26) reduced glomerular filtration rate without altering blood pressure or renin activity, in contrast to the blockade of Cx37 and Cx40 [38]. Moreover, endothelial-specific deletion of Cx43 had no effect on renin secretion and blood pressure in contrast to mice deficient in Cx40 [39].

Connexin43 in experimental CKD

The above mentioned studies established the fact that Cx43 is expressed in the renal parenchyma and the vasculature under resting and/or pathological conditions in both animals and humans. Given its important role in cell communication and signaling it was not long before the role of Cx43 in renal pathology began to be investigated.

Renal vasculature

Renal vasculature is anatomically involved in many nephropathies resulting in CKD including hypertensive nephropathy, vascular stenosis, ischemic nephropathy, and vasculitis. Cx43 has been extensively studied in vascular pathophysiology. As reviewed elsewhere, it appears to be important for the regulation of the myogenic tone and the proliferation and migration of vascular smooth muscle cells (VSMC) [40]. In the renal vasculature Cx43 localizes, apart from VSMCs, in endothelial cells of the renal, lobar, arcuate, and interlobular arteries and afferent and efferent arterioles [41]. As mentioned above, a role for Cx43 in renin secretion and control of blood pressure has also been reported but findings are still contradicting.

To study the role of Cx43 in hypertensive CKD, we used a renin transgenic mouse model (RenTg) that overexpresses renin in the liver, causing a rapid increase of blood pressure and a slowly progressive deterioration of renal function, thus mimicking kinetics in human disease [42, 43]. Renin overexpression gradually induced Cx43 which localized in peritubular and glomerular capillaries and correlated with the severity of the disease [44]. Alonso et al. have demonstrated than in aortic smooth muscle cells, angiotensin II induced Cx43 expression by driving NF-κB binding to Cx43 promoter [45]. To examine the potentially functional role of Cx43 upregulation, we crossed RenTg mice with Cx43 heterozygous mice (Cx43+/-) and monitored the effect of Cx43 downregulation on the progression of the disease [46]. Partial deletion of Cx43 had no effect on blood pressure, supporting the notion that it is not implicated in blood pressure regulation. However, it significantly reduced albuminuria, inflammatory infiltrates and interstitial fibrosis. The protection from the progression of renal disease in this model was subsequently associated to a reduced interaction between endothelial and inflammatory cells. Incubation of endothelial cells with Cx43 blocking peptides reduced monocyte adhesion to the endothelial layer. Pre-incubation of monocytes with the same blocker yielded similar decreased adhesive capacity of monocytes on the endothelium. ATP release, an activator of purinergic cell membrane receptors, has been reported as a means of crosstalk between infiltrating cells and activated endothelium [47], generating pro-inflammatory signals and upregulation of monocytes adhesion molecules [48]. Cx43 has been described to mediate ATP release in several systems including neutrophils [47], microglia [49], retinal pigment epithelial cells [50], inflammatory cells [51] and proximal tubular epithelial cells [52]. Upregulation of Cx43 in renal endothelial cells could promote CKD by generating a pro-inflammatory environment that promotes leukocyte adhesion and infiltration through activation of purinergic signaling.

The podocyte

Yaoita et al. were the first to demonstrate that Cx43 is upregulated in experimental models of glomerular renal disease. Using the puromycin aminonucleoside (PAN) nephrosis model in rats, they showed that injured podocytes strongly expressed Cx43 while its expression in mesangial and glomerular endothelial cells remained unchanged [53]. Even though they provided no evidence for the role of Cx43 in podocyte pathology, they were the first to support the idea that although in basal conditions there are no gap junctions between podocytes, accumulation of Cx43 in podocytes under pathological conditions could indicate the formation of communication channels between neighboring cells. After this report, it was only nine years later when Cx43 was reintroduced in experimental nephropathy. In 2011, our group published a study on the expression of Cx43 in different models of CKD. Among other findings, we showed that in the model of nephrotoxic serum-induced glomerulonephritis (NTS-GN) in mice, Cx43 was strongly upregulated in suffering glomeruli [44]. A year later, an in vitro study on murine podocytes exposed to PAN pointed towards a deleterious role of Cx43 in injured podocytes [54]. Treatment of cultured podocytes with PAN induced Cx43 mRNA and protein expression and increased ROS production via NADPH activation. Gap junctions’ inhibitors reduced caspace-3 activation and restored cell viability, indicating that newly formed gap junctions and/or hemichannels propagate pro-apoptotic signals in response to stress. Similar results were reported with an in vitro system of aldosterone-induced podocyte damage [55]. Aldosterone treatment increased Cx43 expression and gap junction formation and promoted podocyte apoptosis. SiRNA against Cx43 reversed ROS production and restored BAX/BCL-2 ratio, indicating that cell stress signals result in cell death via Cx43-mediated signaling.

Despite the increasing in vitro evidence for the role of Cx43 in podocyte pathophysiology, its in vivo importance for the progression of CKD had not yet been demonstrated. We studied Cx43 expression in biopsies from patients suffering from different types of GN including IgA and C3-GN and found a strong upregulation of Cx43 in the glomerulus [56]. To investigate whether this upregulation is related to the progression of the disease, we used the Cx43+/-mice in the NTS-GN model of CKD. Cx43 was strongly upregulated from early on in the progression of the disease and was de novo expressed by suffering podocytes [56]. Chromatin immunoprecipitation assays revealed that Cx43 upregulation was mediated by c-Jun and STAT1 binding on Cx43 promoter but not by NF-κB as previously reported in challenged arteries [45]. Cx43+/- mice showed more preserved renal function and glomerular structure vs. wild type mice, accompanied by less podocyte apoptosis, inflammatory infiltrates and fibrosis [56]. Mechanistically, we were able to demonstrate in vitro that Cx43 signaling was not restricted to promoting apoptosis. TGF-β induced phenotypic changes to cultured podocytes associated with increased expression of mesenchymal and migratory markers. Blockade of either Cx43 or purinergic signaling resulted in similar reversal of TGF-β-induced alterations, directing towards a cross-talk between ATP signaling and Cx43 deleterious actions [56]. Podocytes express a wide range of purinergic receptors including P2Y2 and P2X7 among others. Extracellular ATP binds to purinergic receptors activating release of Ca+2 from intracellular stores leading to podocyte depolarization [57]. In vivo imaging studies have demonstrated that propagation of Ca+2 waves occurs through gap junctions and mediates several pathogenic responses in the glomerulus including contraction of the glomerular tuft, increased capillary albumin permeability and acquisition of a migratory phenotype of podocytes [58].

Cx43 upregulation in stressed podocytes appears to be stimuli-independent. PAN and aldosterone mediate podocyte toxicity, while the NTS model induces inflammation and altered renal hemodynamics. In a recent study in rats suffering from obesity-related glomerulopathy, Zhao et al. demonstrated increased Cx43 expression that paralleled renal inflammation [59], while increased glomerular, probably podocyte expression of Cx43 has also been reported in a rat model of type-2 diabetes [60]. On the contrary, another study on type 2 diabetes and overt nephropathy patients has correlated the downregulation and redistribution of Cx43 expression in biopsies to the decline of renal function [61]. Conclusively, existing data indicate that the deleterious role of Cx43 in CKD may exceed its pro-inflammatory and pro-apoptotic actions. De novo expression and/or redistribution of Cx43 by suffering cells may induce responses to pathogenic stimuli and phenotypic alterations that are not yet fully understood and promote the disease in different ways.

Mesangial cells

Mesangial cells are contractile cells of the glomerulus that are in contact with other mesangial or endothelial cells via gap junctions [62]. They are considered of great importance since they maintain the glomerular structure by supporting glomerular capillaries and podocytes and regulating glomerular matrix turnover [63]. Mesangioproliferative GN, especially IgA, and diabetic nephropathy are the main types of CKD related to mesangial cells.

Using the anti-Thy 1.1 model of GN in rats, Morioka et al. demonstrated a differential regulation of Cx43 in mesangial cells vs. podocytes. While the podocyte expression of Cx43 increased in animals with GN, it decreased in mesangial cells, showing that Cx43 upregulation is not a universal response to injury in all renal cell populations [64]. In agreement with this study, exposure of cultured mesangial cells to high glucose [65] or aldosterone [66] decreased the expression of Cx43 and induced cytoskeletal rearrangements and proliferation, respectively. The effect of Cx43 on mesangial proliferation, one of the basic histological findings in IgA nephropathy, was attributed to the function of Cx43 hemichannels, since aldosterone had no effect on gap junction formation. Transient overexpression of Cx43 abolished the pro-proliferating effect of aldosterone possibly via Ca+2/Protein kinase C-related signaling [66]. Treatment of mesangial cells with high glucose, a commonly used in vitro model to mimic diabetic nephropathy, resulted in RhoA/ROCK-mediated cytoskeletal rearrangements, translocation of NF-κB to the nucleus, F-actin accumulation and an enhanced interaction between zonula occludens-1 (ZO-1) and Cx43. Interestingly, Cx43 overexpression reversed NF-κB nuclear translocation, while ZO-1 depletion or disruption of F-actin formation prevented the reduction of Cx43 levels induced by high glucose [65]. This indicated the existence of a complex relationship between mesangial cytoskeletal proteins and NF-κB that cross-talks with Cx43 signaling. Collectively, the above studies in mesangial cells argue for a protective role of Cx43 in these cells, which could be exploited in regards of diabetic and IgA nephropathy where the mesangium is of primary importance. In contrast, Solini et al. have shown that changes in extracellular ATP levels, known to be controlled by the function of Cx43, regulate mesangial matrix expansion via a TGF-β-P2X7 pathway [67]. Further in vivo studies employing the appropriate experimental nephropathy models combined with systemic or conditional manipulation of Cx43 expression seem to be necessary to definitely uncover the functional role of Cx43 in mesangial cell-related CKD.

Tubular epithelium

Renal tubular epithelial cells are the primary or secondary target in many forms of CKD. Obstructive nephropathy and renal ischemia have a direct impact on the renal epithelium while diabetic nephropathy, hypertensive nephropathy and GN progressively impair tubules as a secondary effect. After Guo et al. reported the expression of Cx43 in tubular segments [68], a number of in vitro studies suggested a possible role for gap junctions/hemichannels in mediating pathological signaling in tubular epithelial cells. In renal ischemia, epithelial cells are the main cell type susceptible to damage. O2 depletion reduces intracellular ATP levels which in turn results in tubular necrosis. Taking into account that Cx43 hemichannels had been related with ATP release, Vergara et al. investigated the role of Cx43 in an in vitro model of ATP depletion in human proximal tubular cells [69]. ATP depletion induced Cx43 mRNA and protein expression and activated hemichannel signaling. This was also accompanied by increased cell death, but no connection between the two effects was demonstrated. Another study in tubular epithelial cells demonstrated an increase of Cx43 expression induced by TGF-β1, which triggered hemichannel function and provoked ATP release that was further linked to increased expression of interleukin 6 and fibronectin [52]. In diabetic nephropathy, secondary hypertension develops in response to chronic exposure to increased glucose concentrations. When exposed to high glucose in vitro, human collecting ducts responded by upregulation of Cx43 and increased Ca+2 signals propagation mediated by Cx43 gap junctions [36].

To study expression and localization of Cx43 in a model of tubular disease in vivo, we used the well-established model of unilateral ureteral obstructive nephropathy (UUO) in mice [44]. Cx43 was barely detected in control tubular cells but after UUO it was strongly expressed in tubules of both cortex and medulla. Cx43+/- mice showed reduced expression of leukocytes adhesion molecules and reduced macrophage infiltration. Pursuing these initial findings, we demonstrated that blocking Cx43 with antisense oligonucleotides blunted the inflammatory response in UUO and partially preserved E-cadherin junctions in tubular cells in vivo [46]. In subsequent in vitro studies, activation of tubular cells with TGF-β induced collagen production, mitogen-activated protein kinases (MAPKs) phosphorylation and expression of Sp1, a pro-fibrotic transcription factor that promotes collagen synthesis [70]. Blocking Cx43 with the GAP26 peptide blocker reduced the TGF-β effects, indicating that second messengers acting via Cx43 signaling are important for the establishment of renal fibrosis. Table 1 summarizes the current understanding of the role of Cx43 in renal diseases.

Table 1.

Physiopathological functions of Cx43 in different in vitro and in vivo models of renal disease

Connexin43 as a therapeutic target against CKD

Over the last years, a great effort has been made towards the discovery of novel and more efficient pharmacological targets to treat renal diseases. Cx43 has emerged as an active player in the progression of CKD, whose inhibition was proven to successfully impede the development of renal disease by arresting the progress of several inflammatory and fibrotic processes. We were among the first to show that Cx43 is upregulated and participates in the progression of renal disease in several animal models of CKD. Moreover, by using Cx43+/-mice we demonstrated that a reduced expression of Cx43 was sufficient to confer protection against hypertensive nephropathy, obstructive nephropathy and GN [46, 56].

Targeted therapeutic approaches to prevent Cx43 signaling involve the use of antisense oligonucleotides (AS-ODNs) and connexin mimetic peptides designed to mimic sequences on extracellular or intracellular loops of connexin proteins. The inhibition of Cx43 by AS-ODNs has been shown to dampen inflammatory responses and promote wound-healing in many tissues including central nervous system [71], skin [72-74], skeletal muscle [75], heart [76], smooth muscle [77, 78] and vascular endothelium [79-81]. Moreover, there are clinical trials using topical application of a gel containing Cx43 AS-ODNs, which have shown a safe and tolerable treatment of skin wounds, venous leg ulcers and diabetic foot ulcers [71]. In our studies, the use of AS-ODNs against Cx43 inhibited renal inflammation and fibrosis and efficiently preserved renal function in animal models of CKD [46, 56]. Notably, in all cases administration of AS-ODNs started as a therapeutic approach after establishment of the disease, which highlights the potency of Cx43 inhibition in the protection against development of renal disease.

Connexin mimetic peptides may function by either blocking the hemichannel opening or the gap junction formation, based on the protein site (intracellular or extracellular) where the peptides are designed to bind. These specific connexin blockers have been preferred the last years in cell culture and animal studies in place of classical global gap junction inhibitors, since their targeted action is more likely to restrict the unwanted effects on physiological functions and establish an effective regulation. The Cx43 mimetic peptides GAP19 (hemichannel blocker) and GAP26 (gap junction blocker) were proven efficient in preventing arrhythmogenesis and death in a genetic mouse model of muscular dystrophy [82], while administration of GAP26 reduced the myocardial infarct size and improved survival of isolated cardiomyocytes in a rat model of myocardial infarction [83]. In another study, Cx43 mimetic peptides significantly reduced swelling, astrocyte proliferation and neuronal loss in a rodent ex vivo model of spinal cord injury [84]. Furthermore, recent promising studies have been reported in mice suffering from myocardial ischemia where Cx43 hemichannels have been selectively inhibited with GAP19 [85]. We have recently demonstrated that blocking Cx43 with the GAP26 peptide in vitro prevented cell responses associated to inflammatory and fibrotic pathways, i.e. it inhibited monocyte adhesion in activated endothelium, it hampered TGF-β-induced responses in tubular cells [46] and it prevented cytoskeletal changes and apoptosis in podocytes [56]. It remains to be established whether Cx43 mimetic peptides can protect against the progression of renal disease in vivo in animal models.

Conclusion and perspectives

CKD reached pandemic proportions and is one of the major causes of death worldwide. Even though significant progress has been made over the last years, our understanding of the complex mechanisms driving the progression of renal disease is still incomplete. Therapeutic interventions are insufficient and especially in advanced stages the only therapeutic option is dialysis or transplantation. Cx43 was recently identified as a novel mediator of renal disease involved in central processes of inflammation and fibrosis, while its inhibition even after the initiation of the disease was capable to attenuate renal damage and preserve renal function in animal models of vascular, tubular and glomerular CKD. In this sense, novel therapies based on the targeted blockade of Cx43 in desirable cell populations may constitute a future option for efficient inhibition of the progression of CKD. Taking into account that targeted blockers of Cx43 are already available, it remains to be investigated whether they exert a protective effect in preclinical models of CKD, with a potential future application into clinical practice.

Disclosure Statement

The authors declare to have no competing interests.

References


  1. Hill NR, Fatoba ST, Oke JL, Hirst JA, O’Callaghan CA, Lasserson DS, Hobbs R: Global Prevalence of Chronic Kidney Disease – A Systematic Review and Meta-Analysis. Plos One 2016; 11:e0158765.


  2. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators: Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 2016; 388: 1545–1602.


  3. Harris RC, Neilson EG: Toward a unified theory of renal progression. Annu Rev Med 2006; 57: 365–380.


  4. López-Novoa JM, Martínez-Salgado C, Rodríguez-Peña AB, López-Hernández FJ: Common pathophysiological mechanisms of chronic kidney disease: therapeutic perspectives. Pharmacol Ther 2010 Oct; 128: 61–81.


  5. Bosco D, Haefliger JA, Meda P: Connexins: key mediators of endocrine function. Physiol Rev 2011; 91: 1393– 1445.


  6. Spray DC, Stern JH, Harris AL, Bennett MV: Gap junctional conductance: comparison of sensitivities to H and Caions. Proc Natl Acad Sci 1982; 79: 441–445.


  7. Zhou JZ, Jiang JX: Gap junction and hemichannel-independent actions of connexins on cell and tissue functions-an update. FEBS Lett 2014; 588: 1186–1192.


  8. Wagner C: Function of connexins in the renal circulation. Kidney Int 2008; 73: 547–555.


  9. Willecke K, Eiberger J, Degen J, Eckardt D, Romualdi A, Güldenagel M, Deutsch U, Söhl G: Structural and functional diversity of connexin genes in the mouse and human genome. Biol Chem 2002; 383: 725–737.


  10. Loewenstein WR, Rose B: The cell–cell channel in the control of growth. Semin Cell Biol 1992; 3: 59–79.


  11. Meda P, Chanson M, Pepper M, Giordano E, Bosco D, Traub O, Willecke K, el Aoumari A, Gros D, Beyer EC, et al: In vivo modulation of connexin 43 gene expression and junctional coupling of pancreatic β-cells. Exp Cell Res 1991; 192: 469–480.


  12. Wallez Y, Huber P: Endothelial adherens and tight junctions in vascular homeostasis, inflammation and angiogenesis. Biochim Biophys Acta 2008; 1778: 794–809.


  13. Vinken M, Decrock E, De Vuyst E, Ponsaerts R, D’hondt C, Bultynck G, Ceelen L, Vanhaecke T, Leybaert L, Rogiers V: Connexins: sensors and regulators of cell cycling. Biochim Biophys Acta 2011; 1815: 13–25.


  14. Batra N, Kar R, Jiang JX: Gap junctions and hemichannels in signal transmission, function and development of bone. Biochim Biophys Acta 2012; 1818: 1909–1918.


  15. Reaume AG, de Sousa PA, Kulkarni S, Langille BL, Zhu D, Davies TC, Juneja SC, Kidder GM, Rossant J: Cardiac malformation in neonatal mice lacking connexin43. Science 1995; 267: 1831–1834.


  16. Krüger O, Maxeiner S, Kim JS, Van Rijen HV, de Bakker JM, Eckardt D, Tiemann K, Lewalter T, Ghanem A, Lüderitz B, Willecke K: Cardiac morphogenetic defects and conduction abnormalities in mice homozygously deficient for connexin40 and heterozygously deficient for connexin45. J Mol Cell Cardiol 2006; 41: 787–797.


  17. Naus CC, Bani-Yaghoub M, Rushlow W, Bechberger JF: Consequences of impaired gap junctional communication in glial cells. Adv Exp Med Biol 1999; 468: 373–381.


  18. Fushiki S, Perez Velazquez JL, Zhang L, Bechberger JF, Carlen PL, Naus CC: Changes in neuronal migration in neocortex of connexin 43 null mutant mice. J Neuropathol Exp Neurol 2003; 62: 304–314.


  19. Kar R, Batra N, Riquelme MA, Jiang JX: Biological role of connexin intercellular channels and hemichannels. Arch Biochem Biophys 2012; 524: 2–15.


  20. Hanner F, Sorensen CM, Holstein-Rathlou NH, Peti-Peterdi J: Connexins and the kidney. Am J Physiol Regul Integr Comp Physiol 2010; 298:R1143–1155.


  21. Hills CE, Price GW, Squires PE: Mind the gap: connexins and cell-cell communication in the diabetic kidney. Diabetologia 2015; 58: 233–241.


  22. Ribeiro-Rodrigues TM, Martins-Marques T, Morel S, Kwak BR, Girão H: Role of connexin 43 in different forms of intercellular communication – gap junctions, extracellular vesicles and tunnelling nanotubes. J Cell Sci 2017; 130: 3619–3630.


  23. Oyamada M, Kimura H, Oyamada Y, Miyamoto A, Ohshika H, Mori M: The expression, phosphorylation, and localization of connexin 43 and gap-junctional intercellular communication during the establishment of a synchronized contraction of cultured neonatal rat cardiac myocytes. Exp Cell Res 1994; 212: 351–358.


  24. Danesh-Meyer HV, Zhang J, Acosta ML, Rupenthal ID, Green CR: Connexin43 in retinal injury and disease. Prog Retin Eye Res 2016; 51: 41–68.


  25. Kwak BR, Veillard N, Pelli G, Mulhaupt F, James RW, Chanson M, Mach F: Reduced connexin43 expression inhibits atherosclerotic lesion formation in low-density lipoprotein receptor-deficient mice. Circulation 2003; 107: 1033–1039.


  26. Freitas-Andrade M, Naus CC: Astrocytes in neuroprotection and neurodegeneration: The role of connexin43 and pannexin1. Neuroscience 2016; 323: 207–221.


  27. Plotkin LI: Connexin 43 hemichannels and intracellular signaling in bone cells. Front Physiol 2014 4; 5: 131.


  28. Chevallier D, Carette D, Segretain D, Gilleron J, Pointis G: Connexin 43 a check-point component of cell proliferation implicated in a wide range of human testis diseases. Cell Mol Life Sci 2013; 70: 1207–1220.


  29. Elzarrad MK, Haroon A, Willecke K, Dobrowolski R, Gillespie MN, Al-Mehdi AB: Connexin-43 upregulation in micrometastases and tumor vasculature and its role in tumor cell attachment to pulmonary endothelium. BMC Med 2008; 6: 20.


  30. Li Z, Zhou Z, Welch DR, Donahue HJ: Expressing connexin 43 in breast cancer cells reduces their metastasis to lungs. Clin Exp Metastasis 2008; 25: 893–901.


  31. Beyer EC, Kistler J, Paul DL, Goodenough DA: Antisera Directed against Connexin43 Peptides React witha 43-kD Protein Localized to Gap Junctions in Myocardium and Other Tissues. J Cell Biol 1989; 108: 595–605.


  32. Barajas L, Liu L, Tucker M: Localization of connexin43 in rat kidney. Kidney Int 1994; 46: 621–626.


  33. Hillis GS, Duthie LA, Brown PA, Simpson JG, MacLeod AM, Haites NE: Upregulation and co-localization of connexin43 and cellular adhesion molecules in inflammatory renal disease. J Pathol 1997; 182: 373–379.


  34. Sawai K, Mukoyama M, Mori K, Yokoi H, Koshikawa M, Yoshioka T, Takeda R, Sugawara A, Kuwahara T, Saleem MA, Ogawa O, Nakao K: Redistribution of connexin43 expression in glomerular podocytes predicts poor renal prognosis in patients with type 2 diabetes and overt nephropathy. Nephrol Dial Transplant 2006; 21: 2472–2477.


  35. Guo YN, Wang JC, Cai GY, Hu X, Cui SY, Lv Y, Yin Z, Fu B, Hong Q, Chen XM: AMPK-mediated downregulation of connexin43 and premature senescence of mesangial cells under high-glucose conditions. Exp Gerontol 2014; 51: 71–81.


  36. Hills CE, Bland R, Wheelans DC, Bennett J, Ronco PM, Squires PE: Glucose-evoked alterations in connexin43-mediated cell-to-cell communication in human collecting duct: a possible role in diabetic nephropathy. Am J Physiol Renal Physiol 2006; 291:F1045–1051.


  37. Haefliger JA, Krattinger N, Martin D, Pedrazzini T, Capponi A, Döring B, Plum A, Charollais A, Willecke K, Meda P: Connexin43-dependent mechanism modulates renin secretion and hypertension. J Clin Invest 2006; 116: 405–413.


  38. Takenaka T, Inoue T, Kanno Y, Okada H, Meaney KR, Hill CE, Suzuki H: Expression and role of connexins in the rat renal vasculature. Kidney Int 2008; 73: 415–422.


  39. Theis M, de Wit C, Schlaeger TM, Eckardt D, Krüger O, Döring B, Risau W, Deutsch U, Pohl U, Willecke K: Endothelium-specific replacement of the connexin43 coding region by a lacZ reporter gene. Genesis 2001; 29: 1–13.


  40. Figueroa XF, Duling BR: Gap junctions in the control of vascular function. Antioxid Redox Signal 2009; 11: 251–266.


  41. Zhang J, Hill CE: Differential connexin expression in preglomerular and postglomerular vasculature: accentuation during diabetes. Kidney Int 2005; 68: 1171–1185.


  42. Caron KM, James LR, Kim HS, Morham SG, Sequeira Lopez ML, Gomez RA, Reudelhuber TL, Smithies O: A genetically clamped renin transgene for the induction of hypertension. Proc Natl Acad Sci 2002; 99: 8248– 8252.


  43. Huby AC, Kavvadas P, Alfieri C, Abed A, Toubas J, Rastaldi MP, Dussaule JC, Chatziantoniou C, Chadjichristos CE: The RenTg mice: a powerful tool to study renin-dependent chronic kidney disease. PLoS One 2012; 7:e52362.


  44. Toubas J, Beck S, Pageaud AL, Huby AC, Mael-Ainin M, Dussaule JC, Chatziantoniou C, Chadjichristos CE: Alteration of connexin expression is an early signal for chronic kidney disease. Am J Physiol Renal Physiol 2011; 301:F24–32.


  45. Alonso F, Krattinger N, Mazzolai L, Simon A, Waeber G, Meda P, Haefliger JA: An angiotensin II- and NF-kappaB-dependent mechanism increases connexin 43 in murine arteries targeted by renin-dependent hypertension. Cardiovasc Res 2010; 87: 166–176.


  46. Abed A, Toubas J, Kavvadas P, Authier F, Cathelin D, Alfieri C, Boffa JJ, Dussaule JC, Chatziantoniou C, Chadjichristos CE: Targeting connexin 43 protects against the progression of experimental chronic kidney disease in mice. Kidney Int 2014; 86: 768–779.


  47. Eltzschig HK, Eckle T, Mager A, Küper N, Karcher C, Weissmüller T, Boengler K, Schulz R, Robson SC, Colgan SP: ATP release from activated neutrophils occurs via connexin 43 and modulates adenosine-dependent endothelial cell function. Circ Res 2006; 99: 1100–1108.


  48. Salmi M, Jalkanen S: Cell-surface enzymes in control of leukocyte trafficking. Nat Rev Immunol 2005; 5: 760–771.


  49. Ma Y, Cao W, Wang L, Jiang J, Nie H, Wang B, Wei X, Ying W: Basal CD38/cyclic ADP-ribose-dependent signaling mediates ATP release and survival of microglia by modulating connexin 43 hemichannels. Glia 2014; 62: 943–955.


  50. Mugisho OO, Green CR, Kho DT, Zhang J, Graham ES, Acosta ML, Rupenthal ID: The inflammasome pathway is amplified and perpetuated in an autocrine manner through connexin43 hemichannel mediated ATP release. Biochim Biophys Acta 2018; 1862: 385–393.


  51. Dosch M, Gerber J, Jebbawi F, Beldi G. Mechanisms of ATP Release by Inflammatory Cells. Int J Mol Sci 2018; 19:E1222.


  52. Hills C, Price GW, Wall MJ, Kaufmann TJ, Chi-Wai Tang S, Yiu WH, Squires PE: Transforming Growth Factor Beta 1 Drives a Switch in Connexin Mediated Cell-to-Cell Communication in Tubular Cells of the Diabetic Kidney. Cell Physiol Biochem 2018; 45: 2369–2388.


  53. Yaoita E, Yao J, Yoshida Y, Morioka T, Nameta M, Takata T, Kamiie J, Fujinaka H, Oite T, Yamamoto T: Up-regulation of connexin43 in glomerular podocytes in response to injury. Am J Pathol 2002; 161: 1597–1606.


  54. Yan Q, Gao K, Chi Y, Li K, Zhu Y, Wan Y, Sun W, Matsue H, Kitamura M, Yao J: NADPH oxidase-mediated upregulation of connexin43 contributes to podocyte injury. Free Radic Biol Med 2012; 53: 1286–1297.


  55. Yang M, Wang B, Li M, Jiang B: Connexin 43 is involved in aldosterone-induced podocyte injury. Cell Physiol Biochem 2014; 34: 1652–1662.


  56. Kavvadas P, Abed A, Poulain C, Authier F, Labéjof LP, Calmont A, Afieri C, Prakoura N, Dussaule JC, Chatziantoniou C, Chadjichristos CE: Decreased Expression of Connexin 43 Blunts the Progression of Experimental GN. J Am Soc Nephrol 2017; 28: 2915–2930.


  57. Fischer KG, Saueressig U, Jacobshagen C, Wichelmann A, Pavenstädt H: Extracellular nucleotides regulate cellular functions of podocytes in culture. Am J Physiol Renal Physiol 2001; 281:F1075–1081.


  58. Burford JL, Villanueva K, Lam L, Riquier-Brison A, Hackl MJ, Pippin J, Shankland SJ, Peti-Peterdi J: Intravital imaging of podocyte calcium in glomerular injury and disease. J Clin Invest 2014; 124: 2050–2058.


  59. Zhao Y, Li G, Wang Y, Liu Z: Alteration of Connexin43 expression in a rat model of obesity-related glomerulopathy. Exp Mol Pathol 2017; 104: 12–18.


  60. Takenaka T, Inoue T, Okada H, Ohno Y, Miyazaki T, Chaston DJ, Hill CE, Suzuki H: Altered gap junctional communication and renal haemodynamics in Zucker fatty rat model of type 2 diabetes. Diabetologia 2011; 54: 2192–2201.


  61. Sawai K, Mukoyama M, Mori K, Yokoi H, Koshikawa M, Yoshioka T, Takeda R, Sugawara A, Kuwahara T, Saleem MA, Ogawa O, Nakao K: Redistribution of connexin43 expression in glomerular podocytes predicts poor renal prognosis in patients with type 2 diabetes and overt nephropathy. Nephrol Dial Transplant 2006; 21: 2472–2477.


  62. Hirschi KK, Burt JM, Hirschi KD, Dai C: Gap junction communication mediates transforming growth factor-beta activation and endothelial-induced mural cell differentiation. Circ Res 2003; 93: 429–437.


  63. Schlöndorff D, Banas B: The mesangial cell revisited: no cell is an island. J Am Soc Nephrol 2009; 20: 1179– 1187.


  64. Morioka T, Okada S, Nameta M, Kamal F, Yanakieva-Georgieva NT, Yao J, Sato A, Piao H, Oite T: Glomerular expression of connexin 40 and connexin 43 in rat experimental glomerulonephritis. Clin Exp Nephrol 2013; 17: 191–204.


  65. Xie X, Chen C, Huang K, Wang S, Hao J, Huang J, Huang H: RhoA/rho kinase signaling reduces connexin43 expression in high glucose-treated glomerular mesangial cells with zonula occludens-1 involvement. Exp Cell Res 2014; 327: 276–286.


  66. Zhang A, Han Y, Wang B, Li S, Gan W: Beyond Gap Junction Channel Function: the Expression of Cx43 Contributes to Aldosterone-Induced Mesangial Cell Proliferation via the ERK1/2 and PKC Pathways. Cell Physiol Biochem 2015; 36: 1210–1222.


  67. Solini A, Iacobini C, Ricci C, Chiozzi P, Amadio L, Pricci F, Di Mario U, Di Virgilio F, Pugliese G. Purinergic modulation of mesangial extracellular matrix production: role in diabetic and other glomerular diseases. Kidney Int 2005; 67: 875–885.


  68. Guo R, Liu L, Barajas L: RT-PCR study of the distribution of connexin 43 mRNA in the glomerulus and renal tubular segments. Am J Physiol 1998; 275:R439–447.


  69. Vergara L, Bao X, Bello-Reuss E, Reuss L: Do connexin 43 gap-junctional hemichannels activate and cause cell damage during ATP depletion of renal-tubule cells? Acta Physiol Scand 2003; 179: 33–38.


  70. Ghayor C, Chadjichristos C, Herrouin JF, Ala-Kokko L, Suske G, Pujol JP, Galera P: Sp3 represses the Sp1-mediated transactivation of the human COL2A1 gene in primary and de-differentiated chondrocytes. J Biol Chem 2001; 276: 36881–36895.


  71. Tonkin RS, Mao Y, O’Carroll SJ, Nicholson LF, Green CR, Gorrie CA, Moalem-Taylor G: Gap junction proteins and their role in spinal cord injury. Front Mol Neurosci 2015; 7: 102.


  72. Becker DL, Thrasivoulou C, Phillips AR: Connexins in wound healing; perspectives in diabetic patients. Biochim Biophys Acta 2012; 1818: 2068–2075.


  73. Coutinho P, Qiu C, Frank S, Tamber K, Becker D: Dynamic changes in connexin expression correlate with key events in the wound healing process. Cell Biol Int 2003; 27: 525–541.


  74. Qiu C, Coutinho P, Frank S, Franke S, Law LY, Martin P, Green CR, Becker DL: Targeting connexin43 expression accelerates the rate of wound repair. Curr Biol 2003; 13: 1697–1703.


  75. Gorbe A, Becker DL, Dux L, Krenacs L, Krenacs T: In differentiating prefusion myoblasts connexin43 gap junction coupling is upregulated before myoblast alignment then reduced in post-mitotic cells. Histochem Cell Biol 2006; 125: 705–716.


  76. Yasui K, Kada K, Hojo M, Lee JK, Kamiya K, Toyama J, Opthof T, Kodama I: Cell-to-cell interaction prevents cell death in cultured neonatal rat ventricular myocytes. Cardiovasc Res 2000; 48: 68–76.


  77. Liao Y, Duling BR: Blockade of connexin 43 expression by stable transfection of antisense cDNA in cultured vascular smooth muscle cells. Antisense Nucleic Acid Drug Dev 2000; 10: 275–281.


  78. Yeh HI, Lupu F, Dupont E, Severs NJ: Upregulation of connexin43 gap junctions between smooth muscle cells after balloon catheter injury in the rat carotid artery. Arterioscler Thromb Vasc Biol 1997; 17: 3174– 3184.


  79. Kwak BR, Pepper MS, Gros DB, Meda P: Inhibition of endothelial wound repair by dominant negative connexin inhibitors. Mol Biol Cell 2001; 12: 831–845.


  80. Ormonde S, Chou CY, Goold L, Petsoglou C, Al-Taie R, Sherwin T, McGhee CN, Green CR: Regulation of connexin43 gap junction protein triggers vascular recovery and healing in human ocular persistent epithelial defect wounds. J Membr Biol 2012; 245: 381–388.


  81. Yeh HI, Lai YJ, Chang HM, Ko YS, Severs NJ, Tsai CH: Multiple connexin expression in regenerating arterial endothelial gap junctions. Arterioscler Thromb Vasc Biol 2000; 20: 1753–1762.


  82. Gonzalez JP, Ramachandran J, Xie LH, Contreras JE, Fraidenraich D: Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice. Sci Rep 2015; 5: 13490.


  83. Hawat G, Benderdour M, Rousseau G, Baroudi G: Connexin 43 mimetic peptide Gap26 confers protection to intact heart against myocardial ischemia injury. Pflugers Arch 2010; 460: 583–592.


  84. O’Carroll SJ, Alkadhi M, Nicholson LF, Green CR: Connexin 43 mimetic peptides reduce swelling, astrogliosis, and neuronal cell death after spinal cord injury. Cell Commun Adhes 2008; 15: 27–42.


  85. Wang N, De Vuyst E, Ponsaerts R, Boengler K, Palacios-Prado N, Wauman J, Lai CP, De Bock M, Decrock E, Bol M, Vinken M, Rogiers V, Tavernier J, Evans WH, Naus CC, Bukauskas FF, Sipido KR, Heusch G, Schulz R, Bultynck G, Leybaert L: Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury. Basic Res Cardiol 2013; 108: 309.

Author Contacts

Dr. Christos E. Chadjichristos

Institut National de la Santé Et de la Recherche Médicale INSERM UMRS 1155, Tenon Hospital

4 rue de la Chine, 75020 Paris (France)

Tel. (331) 56016680, Fax (331) 56016659, E-Mail [email protected]


Article / Publication Details

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Received: January 18, 2018
Accepted: August 27, 2018
Published online: September 07, 2018

Issue release date: October 2018


Number of Print Pages: 12

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Number of Tables: 1


ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)


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Relationship between changes in blood pressure and morphofunctional changes in the heart in young athletes | Balykova

1. Trachsel L. D., Carlen F., Brugger N., Seiler C., Wilhelm M. Masked hypertension and cardiac remodeling in middle-aged endurance athletes. J Hypertens 2015; 33 (6): 1276-1283. DOI: 10.1097 / HJH.0000000000000558

2.Lin J., Wang F., Weiner R.B., DeLuca J.R., Wasfy M.M., Berkstresser B. et al. Blood Pressure and LV Remodeling Among American-Style Football Players. JACC Cardiovasc Imaging 2016; 9 (12): 1367-1376. DOI: 10.1016 / j.jcmg.2016.07.013

3. Małek A.A., Czajkowska A., Mróz A., Witek K., Barczuk-Falęcka M., Nowicki D. et al. Left ventricular hypertrophy in middle-aged endurance athletes: is it blood pressure related? Blood Press Monit 2019; 24: (3): 110-113.DOI: 10.1097 / MBP.0000000000000377

4. Pressler A., ​​Jähnig A., Halle M., Haller B. Blood pressure response to maximal dynamic exercise testing in an athletic population. J Hypertens 2018; 36 (9): 1803-1809. DOI: 10.1097 / HJH.0000000000001791

5. Zmijewski P., Cięszczyk P., Ahmetov I.I., Gronek P., Lulińska-Kuklik E., Dornowski M.et al. The NOS3 G894T (rs1799983) and -786T / C (rs2070744) polymorphisms are associated with elite swimmer status. Biol Sport 2018; 35 (4): 313-319. DOI: 10.5114 / biolsport.2018.76528

6. Harmon K., Asif I., Maleszewski J., Owens J.S., Prutkin D.M., Salerno J.C. et al. Incidence and Etiology of Sudden Cardiac Arrest and Death in High School Athletes in the United States. Mayo Clin Proc 2016; 91 (11): 1493-1502. DOI: 10.1016 / j.mayocp.2016.07.021

7. Elliott P. M., Anastasakis A., Borger M. A., Borggrefe M., Cecchi F., Charron P. et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: The Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J 2014; 35 (39): 2733-2779. Doi: 10.1093 / eurheartj / ehu284

8.Carbone A., d’Andrea A., Riegler L., Scarafile R., Pezzullo E., Martone F. et al. Cardiac damage in athlete’s heart: When the “supernormal” heart fails! World J Cardiol 2017; 9 (6): 470– 480. DOI: 10.4330 / wjc.v9.i6.470

9. Smolensky A.V., Mikhailova A.V., Tatarinova A.Yu. Arterial hypertension in athletes and sports heart remodeling. International Journal of Heart and Vascular Diseases 2017; 14 (5): 36–45.[Smolenskij A.V., Mihajlova A.V., Tatarinova A.Yu. Hypertension in athletes and remodeling of a sports heart. Mezhdunarodnyi zhurnal serdtsa i sosudistykh zabolevanii (International Journal of Heart and Vascular Diseases) 2017; 14 (5): 36–45. (in Russ.)]

10. Barbitoff Y.A., Bezdvornykh I.V., Polev D.E., Serebryakova E.A., Glotov A.S., Glotov O.S., Predeus A.V. Catching hidden variation: Systematic correction of reference minor allele annotation in clinical variant calling.Genetics in Medicine 2018; 20 (3): 360-364. DOI: 10.1038 / gim.2017.168

11. Gurevich T.S., Matveev S.V., Kirillov D.A. Early echocardiographic signs of cardiovascular overstrain in athletes (diagnostics, rehabilitation). Physiotherapy and sports medicine 2012; 6: 15-19. [Gurevich T.S., Matveev S.V., Kirillov D.A. Early echocardiographic signs of cardiovascular overstrain in athletes (diagnosis, rehabilitation).Lechebnaya fizkul’tura i sportivnaya meditsina 2012; 6: 15-19. (in Russ.)]

12. Makarov L.M., Fedina N.N., Komolyatova V.N., Bezprotochny D.A., Kiseleva I.I. Standard parameters of blood pressure in young elite athletes during a test with dosed physical activity. Pediatrics. Journal named after G.N. Speransky 2015; 94 (2): 102-104. [Makarov L.M., Fedina N.N., Komoljatova V.N., Besprotochnyj D.A., Kiseljova I.I. Normal values ​​of blood pressure in young elite athletes during an exercise test. Pediatriya. Zhurnal im. G.N. Speranskogo (Pediatria. Journal named after G.N. Speransky) 2015; 94: (2): 102-104 (in Russ.)]

13. Shirokova A.A., Balykova L.A., Ivyansky S.A., Varlashina K.N., Soldatov Yu.O., Kazankina V.S. and others. Possibilities of daily monitoring of blood pressure and tests with dosed physical activity in the diagnosis of arterial hypertension in young athletes.Practical Medicine 2019; 17 (2): 74-79. [Shirokova A.A., Balykova L.A., Ivjanskij S.A., Varlashina K.N., Soldatov Yu.O., Kazankina V.S. et al. 24-hour monitoring of blood pressure and exercise tests in the diagnosis of arterial hypertension in young athletes. Prakticheskaya meditsina 2019; 17 (2): 74-79. (in Russ.)

14. Balykova L.A., Ivyanskiy S.A., Urzyaeva A.N. Metabolic therapy in pediatric sports cardiology.Heart and sport in children and adolescents: problems of “interaction”. Ed. E.A. Diagtereva. M., 2011; 199-213. [Balykova L.A., Ivyansky S.A., Urzyaeva A.N. Metabolic therapy in pediatric sports cardiology. Heart and sport in children and adolescents: problems of “interaction”. E.A. Dyagtereva (ed.). Moscow, 2011; 199-213. (in Russ.)]

15. Brady T.M. Obesity-Related Hypertension in Children. Front Pediatr. 2017; 5: 197.DOI: 10.3389 / fped.2017.00197

16. Balykova L.A., Ivyansky S.A., Shchekina N.V., Mikheeva K.N., Urzyaeva A.N. Arterial hypertension in children athletes. Russian Bulletin of Perinatology and Pediatrics 2015; 60 (6): 48-54. [Balykova L.A., Ivjanskij S.A., Shhekina N.V., Miheeva K.N., Urzjaeva A.N. Arterial hypertension in young athletes. Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 2015; 60 (6): 48–54 (in Russ.)]

17. Rowland T., American College of Sports Medicine, North American Society for Pediatric Exercise Medicine (NASPEM). Cardiopulmonary Exercise Testing in Children and Adolescents. United States of America, 2017; 65-79.

18. Caselli S., Serdoz A., Mango F., Lemme E., Vaquer Seguì A., Milan A. et al. High blood pressure response to exercise predicts future development of hypertension in young athletes.Eur Heart J 2019; 40 (1): 62–68. DOI: 10.1093 / eurheartj / ehy810

19. Leischik R., Spelsberg N., Niggemann H., Dworrak B., Tiroch K. Exercise-induced arterial hypertension – an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes? F1000Res 2014; 3: 105. DOI: 10.12688 / f1000research.4001.1

20.Lovic D., Narayan P., Pittaras A., Faselis Ch., Doumas M., Kokkinos P. et al. Left ventricular hypertrophy in athletes and hypertensive patients. J Clin Hypertens (Greenwich) 2017; 19 (4): 413-417. DOI: 10.1111 / jch.12977

21. Wang X., Chandrashekar K., Wang L., Lai E. Y., Wei J., Zhang G. et al. Inhibition of Nitric Oxide Synthase 1 Induces Salt-Sensitive Hypertension in Nitric Oxide Synthase 1α Knockout and Wild-Type Mice.Hypertension 2016; 67 (4): 792-799. DOI: 10.1161 / HYPERTENSIONAHA.115.07032

22. Gomez A.T., Prutkin J.M., Rao A.L. Evaluation and Management of Athletes With Long QT Syndrome. Sports Health 2016; 8 (6): 527-535. DOI: 10.1177 / 1941738116660294

Normal blood pressure: reference table

Normal blood pressure: reference table

Age / Gender

Men

Women

top

lower

top

lower

Newborn

70

1 year

96

66

95

65

10 years

103

69

103

70

20 years

123

76

116

72

30 years

126

79

120

75

40 years

129

81

127

80

50 years

135

83

137

84

60 years

142

85

144

85

70 years

145

82

159

85

80 years

147

82

157

83

90 years

145

78

150

79

Read more:

Blood pressure

If you have high blood pressure

If you have an increase in blood pressure, it is very important to immediately understand that a large proportion of successful treatment depends not only on the doctor and medications, but also on your own attitude to the disease and strict adherence to recommendations.

If you have an increase in blood pressure, it is very important to immediately understand that a large proportion of successful treatment depends not only on the doctor and medications, but also on your own attitude to the disease and strict adherence to recommendations.

Why is it important for the doctor and patient to be allies in the treatment of hypertension? A number of factors closely related to lifestyle and habits contribute to an increase in pressure: unhealthy diet, smoking, lack of physical activity, psycho-emotional overstrain.

Hypertension develops 6 times more often in people who eat irrationally, abuse fatty and salty foods, alcohol, and are overweight. Stressful situations, and especially an inappropriate response, can also be attributed to adverse health factors.

Normalization of weight, a sufficient level of adequate physical daily activity, rejection of bad habits, rational nutrition can lead to a decrease in high blood pressure.

Rule No. 1

Monitor blood pressure regularly

Regardless of age, monitor your blood pressure.

For information:

According to the latest recommendations of the World Health Organization, blood pressure levels below 120/80 mm Hg are considered normal. Art., the pressure level is between 120/80 and 140/90 mm Hg. Art. refers to high normal (this is already a risk zone), and the pressure is 140/90 mm Hg. Art. and above is considered arterial hypertension.

Most people with hypertension have a moderate increase in blood pressure and do not present health complaints, but an asymptomatic course does not mean the absence of the disease.

Check how often your blood pressure will change during the day, what is the initial level in the morning, in the evening, during the day, week.

With a graphical representation of your pressure level, it will be easier for your doctor to select the drug and its dose, taking into account your individual characteristics.

Rule No. 2

Follow the principles of good nutrition

Remember: Overweight, if it is not associated with any disease, most often develops as a result of systematic overeating, and not as a result of “gluttony”, but as a result of irregular “snacks”, a systematic discrepancy between energy expenditure and energy intake.With a regular excess of the daily caloric content of food over energy consumption, for example, by 200 kcal per day, body weight may increase by 3-7 kg per year.

First of all, you need to know what weight is normal for you, and what is overweight. For ease of determining whether you are overweight, you can focus on the formula for men “height-100”, for women “height-105”.

It is most reasonable to start normalizing your weight by revising your habits and nutritional composition, to lose a few extra pounds, and only then, to achieve a more stable normal weight, you can start training physical activities.

It is very important to maintain a balance between the energy that we receive from food and the energy expenditure of the body. A middle-aged person, especially if he has high blood pressure, should not be overweight.

Rational nutrition is nutrition that contributes to maintaining health, satisfies the needs of our body for nutrients, vitamins, minerals,
energy.

For information: The daily protein requirement of is 90-95 g.It is recommended to regularly combine foods containing animal protein (1/3 daily protein) and vegetable protein (2/3 daily protein).

Complete protein is found in all animal products – meat, fish, poultry, dairy products (cottage cheese, cheese, milk), eggs.

Sources of vegetable protein – legumes, nuts, potatoes, grain products.

Daily fat requirement is 80-100 g.

About half of this amount is found in products (meat, cheese, cottage cheese, milk, etc.)etc.).

For cooking, dressing salads, cereals, sandwiches, it is recommended not more than 40-50 g of fat per day (3 tablespoons, preferably in a 1: 2 ratio of animal and vegetable fat).

Vegetable fats (sunflower, corn, cottonseed oil), fish, seafood also contain substances useful for normalizing high blood pressure, fat-soluble vitamins (A, groups B, C, P).

Fat of marine fish contains polyunsaturated fatty acids useful in hypertension and atherosclerosis.

The daily requirement for carbohydrates is 300-350 g.

Carbohydrates are complex and simple.

The main part (up to 300 g) must be absorbed by complex carbohydrates. These are starchy foods – bread, cereals, pasta, potatoes, as well as vegetables and fruits.

Simple carbohydrates (sugar in its pure form and contained in sweets, sweet drinks) are recommended no more than 40 g per day.

You should limit consumption of table salt to 5 g (a teaspoon without top) per day and increase the consumption of foods rich in potassium salts to 5-6 g.

Products with a low sodium content (up to 0.1 g per 100 g of product) – natural products of plant origin, cottage cheese, fish, meat. Gastronomic (ready-made) foods contain significantly more salt than natural ones. For example, sausage and cheese contains 10-15 times more salt than natural meat.

Significant amount of Potassium (more than 0.5 g per 100 g of product), is contained in apricots, beans, seaweed, prunes, raisins, peas, potatoes (baked in “jacket”).Also, a lot of potassium (up to 0.4 g per 100 g) contains beef, pork, cod, hake, mackerel, squid, oatmeal, green peas, tomatoes, beets, radishes, green onions, currants, grapes, apricots, peaches.

Vegetables, fruits, and especially berries, as well as other plant products contain a lot of useful fiber , vitamins and mineral salts (potassium, magnesium). Mineral salts and substances that reduce pressure are found in beets, onions, garlic, sowing lettuce, black currants, black chokeberries, lingonberries, and wild strawberries.

Rule No. 3

Strive to increase physical activity

Your doctor will determine the level of acceptable physical activity if you want to do special training. The goal of increasing physical activity should be considered the achievement of the training effect of training. It is most rational if you set a real goal for yourself – to increase daily physical activity in the normal rhythm of life.

The basics of self-control will help you in all cases:

To determine the effect of physical activity on your body, you should monitor the pulse before and after the load and determine the time during which the pulse is restored to baseline after the same load, for example, after 20 squats.

At the height of the load, the pulse should not exceed 120-140 in 1 minute (180 minus age in years).

Classes should not provoke shortness of breath, profuse sweating, general weakness, pain in the heart. The appearance of these symptoms indicates the inadequacy of the loads and is a signal for reducing the intensity of the load and re-consulting a doctor.

The training effect of loads is manifested in a decrease in the heart rate in a calm state and a gradual reduction in the recovery time of the pulse after exercise (20 squats).If your state of health deteriorates (sleep, appetite, performance are disturbed, discomfort appears), then this will require a reduction in stress and a second consultation with a doctor.

Rule No. 4

Try to get rid of bad habits

Smoking and alcohol abuse have a negative impact on health. Nicotine contained in cigarette smoke excites, increases the load on the heart, causes vasoconstriction, and increases blood pressure.

Under the influence of alcohol, control over the state of health is lost, an increase in pressure becomes more dangerous.

Rule No. 5

Learn to deal with stressful situations

You can easily learn how to reduce psycho-emotional stress (stress). Ways of mental regulation will help you: breathing training, volitional muscle relaxation, changing body position, concentration of attention, and sometimes simple rest.

It is almost impossible to avoid many conflict situations, but it is possible to learn how to treat and neutralize them correctly.

The worst way to “discharge” is to rip off resentment and anger on people close to you. The harm from this is twofold.

Avoid a state of overwork, especially a chronic one, alternate between mental and physical work.

You should have a good rest, sleep at least 8-9 hours a day. It is imperative to adjust the physiological circadian rhythm – the alternation of hours of wakefulness (day) and sleep (night).

Practical advice:

Some “nonspecific” remedies may be helpful to you to help you fall asleep (a calm walk in the fresh air, a warm foot bath or a shared bath, refusal of a hearty dinner in the evening, refusal of television programs). Do not forget about well-proven traditional medicine, herbs (valerian, St. John’s wort).

When you find yourself in an unpleasant situation that worries you, pause before expressing your anger, discontent, change the topic of conversation, do not make hasty decisions.

Rule No. 6

Strictly follow all doctor’s advice!

If your doctor prescribes medication for you, it is important that you strictly follow his recommendations.

All tips described in these rules are not short-term recommendations for you. You need to embrace them as a new, healthier lifestyle and new habits.

If your blood pressure rises slightly, then following these rules can save you from the disease.

If the pressure is prone to significant and prolonged rises, and you need to take medications as prescribed by a doctor, then following these tips will help you to quickly reduce the pressure, reduce the dose of drugs.

You can significantly help yourself, regardless of the cause of hypertension, if you know a few simple but important rules and follow them.

These tips do not require significant time and money.

You should accept them as a new, healthier lifestyle and new habits, which will require the mobilization of willpower, and therefore your active efforts.

90,000 Post-Loop Approach: Health Test

In the Upper Volga region, as well as throughout the country as a whole, in accordance with the decree of the Government of the Russian Federation, a program of in-depth medical examination for post-ovid patients has been launched.

Today, doctors are increasingly talking about the fact that coronavirus is not a simple infectious disease, it affects almost all body systems. According to the WHO, every tenth person who has had covid, even after 3 months, suffers from any consequences – from unrecoverable sense of smell to thrombosis.

According to the latest data, the number of patients in the Tver region exceeded 56 thousand people. And all of them can be examined for free. To do this, you need to contact the polyclinic at the place of residence, preferably not earlier than 2 months after the illness. The new medical service is included in the territorial program of state guarantees.

– Advanced prophylactic medical examination is a complex of additional examinations, more complex and technologically advanced types of diagnostics, which allow assessing the condition of the postcoid patient, identifying the consequences and complications, as well as developing an individual plan for rehabilitation and treatment, – said the chief physician of the regional clinical treatment and rehabilitation center Alexander Startsev.-

– Coronavirus infection violates all laws of infectious diseases. We often neglect the means of protection, the possibility of being vaccinated, and the consequences can be very serious. Therefore, it is important to identify them in time and undergo treatment.

According to him, even a mild coronavirus can lead to changes in the lungs, thrombosis, impaired blood pressure, respiratory failure and damage to the cardiovascular and even nervous system. And such a common symptom as loss of smell, just speaks of problems in the central nervous system.

Clinical examination traditionally takes place in two stages. After examining the therapist, the patient does a general and biochemical blood test, a walking test, blood oxygen saturation, etc. If necessary, if there are risks or signs of any consequences, the person undergoes additional studies, such as computed tomography, Doppler examination of the vessels of the lower extremities, echocardiography …

Irina TURINA

90,000 Prices for a number of drugs and products have changed in Russia

MOSCOW, Aug 6 – PRIME. Rosstat published a number of data on changes in prices for food and drugs in Russia in July, follows from the message of the statistical department of the Russian Federation.

PRODUCTS

Cabbage in Russia in July rose in price by 10.8% compared to June of the current year, garlic – by 2.8%; at the same time, potatoes fell in price by 20.3%, beets – by 16.6%, onions – by 8.1%, carrots – by 4.6%, according to the materials.

“In July, a significant impact on the dynamics of prices was made by the cheapening of fruits and vegetables.So, potatoes fell in price by 20.3%, cucumbers – by 19.5%, tomatoes – by 17.9%, beets – by 16.6%, onions – by 8.1%, bananas – by 5.7%, carrots – by 4.6% “, – according to the statistical office.

In addition, the cost of grapes decreased by 2.5%, fresh mushrooms – by 2.3%. “At the same time, prices for white cabbage rose by 10.8%, garlic – by 2.8%, dried fruits – by 1.2%, apples and oranges – by 0.9%,” adds Rosstat.

Building materials are becoming more expensive in Russia

Prices for beets in 18 regions decreased by 0.1-9.9%, in 12 regions – by 10-19.9%, in 10 – by 20-29.9%, in another 10 – by 30-63, 6%.In turn, in 18 regions the price for beets increased by 0.1-9.9%, in 17 regions – by 10.0-51.8%. Potatoes in 12 regions fell by 0.1-9.9%, in 28 – by 10-19.9%, in 23 – by 20-29.9%, in 10 – by 30-46.5%. In the Chukotka Autonomous Okrug, prices have not changed.

In eight constituent entities of the Russian Federation, prices for potatoes increased by 0.1-9.9%, in three – by 10-23.8%. Cucumber prices in eight regions decreased by 0.1-9.9%, in 26 regions – by 10-19.9%, in 35 regions – by 20-29.9%, in 13 regions – by 30-44, five%. In three constituent entities of the Russian Federation, prices for cucumbers increased by 0.1-33.3%, the report says.

Tomatoes in 10 regions fell by 0.1-9.9%, in 42 – by 10-19.9%, in 24 – by 20-29.9%, in eight – by 30-45.5%. In the Sakhalin region, tomatoes have risen in price by 8.1%.

“Prices for carrots in 23 constituent entities of the Russian Federation decreased by 0.1-9.9%, in 10 constituent entities – by 10-19.9%, in seven constituent entities – by 20-41.6%. In 25 constituent entities, prices for carrots grew by 0.1-9.9%, in 12 regions – by 10-19.9%, in eight regions – by 20-78.4%, “Rosstat adds.

Fish in July of this year has risen in price by 2.1% compared to June, red caviar – by 1.4%, ice cream – by 1.3%, sugar – by 0.5%, sunflower oil – by 0.4% , follows from the materials of Rosstat.

In general, bread and bakery products in Russia in July rose by 0.43% compared to June (by December of last year – by 4.05%, compared to July 2020 – by 7.84%), cereals and legumes – by 0.66% (by the beginning of the year – by 5.58%, in annual terms – by 7.65%), pasta – by 0.79% (compared to the beginning of the year – by 4.88%, in in annual terms – by 8.29%).

Meat and poultry became more expensive by 0.56% compared to June (compared to the beginning of the year – by 9.65%, in annual terms – by 11.43%), fish and seafood – by 0.68% (by compared to the beginning of the year – by 6.29%, in annual terms – by 9.78%), milk and dairy products – by 0.45% (compared to the beginning of the year – by 2.84%, in annual terms – by 4.36%), butter – by 0.29% (by the beginning of the year – by 2.9%, in annual terms – by 4.92%).

“Among other food products, prices went up: live and chilled fish – by 2.1%, beef liver, salmon caviar, mayonnaise – by 1.4-1.8%,” the statistics department reports. Prices for granulated sugar in Russia on average increased by 0.5%, the increase in prices for sunflower oil amounted to 0.4%. Chicken eggs fell 2.2%.

“Among other food products, prices fell: fruit juices – by 0.5%, olive oil – by 0.3%, lamb (except for boneless meat), frozen shrimps, coffee beans or ground coffee – by 0.2%, millet, tea, beer – by 0.1% “, – adds Rosstat.

Prices for canned meat for baby food and canned fish in tomato sauce, chicken legs, salted, pickled, smoked fish, processed cheeses, buckwheat, fat cottage cheese, ice cream, soft candies glazed with chocolate, cookies, muffins, rolls, dry soups in packages increased by 1.0-1.3%.

In addition, in July, prices for pork, smoked meats, chilled and frozen cut salmon fish, herring fillets, natural canned fish and canned food with the addition of butter, margarine, national cheeses and feta cheese, curd cheeses glazed with chocolate, condensed milk with sugar, vegetable canned food for baby food, semolina, oat and pearl barley, peas and beans, pasta made from premium wheat flour, cocoa, salt, cereal flakes (by 0.7-0.9%).

MEDICINES

Corvalol, a sedative drug based on phenobarbital, often used by elderly people with heart disease, rose 1.8% in July compared to June, troxerutin, a drug for treating veins, by 2%, according to Rosstat data.

Russia proposed to reduce the list of over-the-counter drugs

“Medicines not related to vital and essential medicinal products (VED) have become more expensive by 0.7%, including troxerutin – by 2%, Corvalol, levomekol – by 1.8%,” Rosstat reports.In general, in July, medicines rose in price versus June by 0.34%, since the beginning of the year – by 2.54%, and compared to July last year – by 6.5%.

Fluocinolone acetonide, an anti-inflammatory drug, and sodium heparin, which is an anticoagulant, rose 1.6%. The price of valocordin, linex, bromhexine, nimesulide, metamizole sodium, known as analgin, allochol, taurine and iodine increased by 0.7-1.3%. Combined analgesics dropped in price by 1.2%, almagel – by 1.1%, validol – by 0.4%.

“Prices for drugs related to vital and essential drugs, on average, have not changed,” the message says. At the same time, ibuprofen rose in price by 0.7%, acetylsalicylic acid (aspirin) – by 0.6%, pancreatin – by 0.5%. Loratadine (antihistamine – ed.), Glycine, smecta, ambroxol, apixaban (anticoagulant – ed.), Drotaverine (antispasmodic – ed.), Loperamide (for the treatment of diarrhea – ed.) Rose in price by 0.2-0.4%.

Within the same range, by 0.2-0.4%, prices for umifenovir, known as arbidol, and chlorhexidine increased.Amoxicillin with clavulanic acid fell by 1.5%, oseltamivir (antiviral drug – ed.) – by 1.2%, suprastin, colecalciferol (vitamin D3) and azithromycin – by 0.2-0.4%.

The State Department also reported that domestic cotton wool in July rose in price by 0.7% compared to June, blood pressure monitors and disposable syringes – by 0.5%, bandages and electronic thermometers – by 0.2%. Mercury-free thermometers using galinstan (an alloy of gallium, indium and tin – ed.) fell 0.9%.

Normal blood pressure and pulse of all ages

What is the normal pressure and pulse of a person – blood pressure (BP) from birth to old age

Normal human arterial blood pressure and pulse. The value of normal blood pressure and pulse depends on the person’s age, individual characteristics, lifestyle, occupation. Blood pressure and pulse are the first signals about the state of human health.All people have normal blood pressure and pulse is different.

Blood pressure is the pressure of blood in a person’s large arteries. There are two indicators of blood pressure:

Systolic (upper) blood pressure is the level of blood pressure at the time of the maximum contraction of the heart.

Diastolic (lower) blood pressure is the level of blood pressure at the time of maximum relaxation of the heart.

Blood pressure is measured in millimeters of mercury, abbreviated as mm Hg.Art. A blood pressure value of 120/80 means that the systolic (upper) pressure is 120 mm Hg. Art., and the value of the diastolic (lower) blood pressure is 80 mm Hg. Art.
Increased numbers on the tonometer are associated with serious diseases, for example, the risk of cerebrovascular accident, heart attack.

In the case of a chronic increase in blood pressure, the risk of stroke increases 7 times, chronic heart failure 6 times, heart attack 4 times and peripheral vascular disease 3 times.

What is normal pressure?

What are its indicators at rest and during physical activity?

Blood pressure is divided into: optimal – 120 to 80 mm Hg. Art., normal – 130 to 85 mm Hg. Art., high, but still normal – from 135-139 mm Hg. Art., at 85-89 mm Hg. Art. A pressure of 140 to 90 mm Hg is considered high. Art. and more. With physical activity, blood pressure rises in accordance with the needs of the body, an increase of 20 mm Hg.Art. speaks of an adequate reaction of the cardiovascular system. If there are changes in the body or risk factors, then with age, blood pressure changes: diastolic pressure rises up to 60 years, and systolic – increases throughout life.

For the accuracy of the results, blood pressure should be measured after 5-10 minutes of rest, and one hour before the examination, do not smoke or drink coffee. During the measurement, the hand should rest comfortably on the table. The cuff is fixed on the shoulder so that its lower edge is 2-3 cm higher than the fold of the elbow fold.In this case, the center of the cuff should be above the brachial artery. When the doctor finishes pumping air into the cuff, he begins to gradually deflate it, and we hear the first tone – systolic.

The classification of the World Health Organization adopted in 1999 is used to assess the level of blood pressure.

Blood pressure category * Systolic (upper) blood pressure mm Hg.Art. Diastolic (lower) blood pressure mm Hg. Art.
Standard
Optimal ** Less than 120 Less than 80
Normal Less than 130 Less than 85
High normal 130-139 85-89
Hypertension
1st stage (soft) 140-159 90-99
2nd degree (moderate) 160-179 100-109
3rd degree (severe) More than 180 More than 110
border 140-149 Less than 90
Isolated systolic hypertension More than 140 Less than 90

* If systolic and diastolic blood pressure are in different categories, the highest category is selected.
** Optimal in relation to the risk of cardiovascular complications and mortality

The terms “mild”, “borderline”, “severe”, “moderate”, given in the classification, characterize only the level of blood pressure, and not the severity of the patient’s disease.
In everyday clinical practice, the classification of arterial hypertension by the World Health Organization, based on the defeat of the so-called target organs, has been adopted. These are the most common complications in the brain, eyes, heart, kidneys and blood vessels.

What should be the normal blood pressure of a person?

K

Which human blood pressure is normal?

The correct answer is as follows: for each person his own norm is .

Indeed, the value of normal blood pressure depends on the age of the person, his individual characteristics, lifestyle, occupation.

Normal newborn pressure is 70mm.Hg
Normal blood pressure in a child who is one year old: boys – 96/66 (upper / lower), girls – 95/65.
Normal blood pressure in a 10-year-old child: 103/69 for boys and 103/70 for girls.

And what is the normal blood pressure of a person who has already matured?

Normal blood pressure in young people 20 years old: in boys – 123/76, in girls – 116/72.

Normal blood pressure in young people who are about 30 years old: in young men – 126/79, in young women – 120/75.

What is the normal blood pressure in a middle-aged person? In 40-year-old men 129/81, in 40-year-old women 127/80.

For fifty-year-old men and women, the normal pressure is 135/83 and 137/84, respectively.
For older people, the following pressure is considered normal: for 60-year-old men 142/85, for women of the same age 144/85.

For older people who have turned 70 years old, the normal pressure is 145/82 for men and 159/85 for women.

What is the normal blood pressure of an old or elderly person? For 80-year-old people, pressure 147/82 and 157/83 for men and women, respectively, is considered normal.

For elderly ninety-year-old grandfathers, normal pressure is 145/78, and for grandmothers of the same age – 150/79 mm Hg.

With unusual physical exertion or emotional stress, the value of blood pressure increases. Sometimes this interferes with doctors when examining cardiac patients, who for the most part are impressionable people.

American scientists even talk about the existence of the so-called “white coat effect”: when the results of measuring blood pressure in a doctor’s office are at 30-40 mm Hg. Art. higher than when you measure it yourself at home. And this is due to the stress that the environment of the medical institution causes in the patient.

On the other hand, in people who are constantly exposed to heavy loads, for example, athletes, a pressure of 100/60 or even 90/50 mm Hg becomes normal.Art. But with all the variety of “normal” blood pressure indicators, each person usually knows the rate of his blood pressure, in any case clearly captures any deviations from it in one direction or another.

There are also certain landmarks of blood pressure that change with age (norms for 1981):

Age 16-20 years old 20 – 40 years old 40 – 60 years old More than 60 years
Upper blood pressure 100-120 120-130 Up to 140 150
Lower blood pressure 70-80 70-80 Up to 90 90

However, modern ideas about normal blood pressure are somewhat different.It is now believed that even a small increase in blood pressure over time can increase the risk of coronary heart disease, stroke and other diseases of the cardiovascular system. Therefore, normal indicators of blood pressure in adults are currently considered to be up to 130-139 / 85-89 mm Hg. Art. The norm for patients with diabetes mellitus is considered to be a pressure of 130/85 mm Hg. Art. An arterial blood pressure of 140/90 is considered high.Blood pressure over 140/90 mm Hg. Art. is already a sign of arterial hypertension.

Normal human heart rate

Pulse (lat. Pulsus blow, push) – periodic fluctuations in the volume of blood vessels associated with contractions of the heart, due to the dynamics of their blood filling and pressure in them during one cardiac cycle. In an average healthy person, a normal 90,049 resting heart rate is 60-80 beats per minute 90,050.

So, the more economical the metabolic processes, the fewer the number of beats the human heart makes per unit of time, the longer the life span.