Exercise-induced hypertension is associated with angiotensin II activity and total nitric oxide

Abstract

Angiotensin II mediates exercise-induced hypertension (EIH), which adversely impacts future cardiovascular health. There is paucity of data on the association between EIH and angiotensin II in well-trained middle-aged marathoners. Therefore, we investigated the renin-angiotensin-aldosterone-system and total nitric oxide activity in middle-aged marathoners with EIH. Seventy middle-aged marathoners were divided into 3 groups: normal blood pressure ([NBPG] [n = 21]), EIH group ([EIHG] [n = 35]), and complex hypertension group ([CHG] [n = 14]). We defined NBPG as resting systolic BP/diastolic BP (SBP/DBP) of ≤140/90 mm Hg and maximal exercise SBP of ≤210 mm Hg, EIHG as resting SBP/DBP ≤140/90 mm Hg and maximal exercise SBP of ≥210 mm Hg, and CHG as resting SBP/DBP ≥140/90 mm Hg and maximal exercise SBP of ≥210 mm Hg. Renin-angiotensin-aldosterone-system and NO levels were measured before and 30 minutes after the graded exercise test. Renin level was elevated while angiotensin level was reduced after 30 minutes of graded exercise test. There was no change in angiotensin I and angiotensin converting enzyme levels. Comparing the groups, renin level was only elevated in the CHG during recovery, while aldosterone level was higher than the baseline level in the recovery phase in all groups. Angiotensin I level remained unchanged in all groups. Angiotensin II level reduced significantly in the NBPG group but remained at the baseline in the EIHG and CHG groups. NO level was unchanged in the NBPG group but reduced in the EIHG and CHG groups after exercise. At 3 minutes of recovery, SBP was the highest in the NBPG group, followed by the EIHG and CHG groups ( P < .05). In conclusion, angiotensin II activity and reduced NO level are associated with EIH in middle-aged long-distance runners. Angiotensin II inhibitors may; therefore, be the more appropriate antihypertensive medication for runners with EIH.

Molecular Mechanisms of Nigella sativa- and Nigella sativa Exercise-Induced Cardiac Hypertrophy in Rats

“…Vigorous or prolonged exercise activity frequently incurs the activation of pathological cardiac pathways and yields elevated biomarkers of cardiac damage [ 33 ]. Furthermore, some competitive long-distance runners developed exercise-induced hypertension, which was associated with an abnormal level of angiotensin-II [ 34 ]. ET-1 was also found elevated significantly in the Ex.…”

Exercise-mediated adaptations in vascular function and structure: Beneficial effects in coronary artery disease

“…The modality by which vascular response to exercise training can be influenced in hypertensive individuals has been studied by the SEFRET study, while in spontaneous hypertensive mice the lack of a positive effect of high intensity exercise on endothelial function was found to be related to NO availability imbalance[ 40 , 41 ]. Kim et al [ 42 ] enrolled middle-aged marathoners with exercise-induced hypertension and reported increased angiotensin II with a reduction in NO levels. These findings may explain the deterioration of arteries vasodilator capacity and elevated blood pressure during exercise in this group of long-distance runners, as well as the therapeutic effect of angiotensin II inhibitors in patients with exercise-induced hypertension.…”

Exercise-Induced Hypertension in Healthy Individuals and Athletes: Is it an Alarming Sign?

“…It has been found that EIH is linked to angiotensin II and nitric oxide (NO) activities during exercise. The renin-angiotensin-aldosterone system (RAAS) changes during and after exercise treadmill test in marathon runners were observed by Chul-Hyun Kim [ 20 ]. The study reported a reduction in angiotensin II and no significant change in NO in people with normal blood pressure after exercise.…”

“…However, angiotensin II remained elevated with a reduction in NO in runners with EIH. Since the RAAS system plays a role in regulating blood pressure, these results may explain the reduction in the vasodilatory effect of arteries, leading to an increase in BP during exercise [ 20 ].…”

“…As discussed previously, the most common pathophysiological mechanisms behind EIH are elevated angiotensin II, reduction in nitric oxide (NO) levels, and an increase in sympathetic tone. Thus, angiotensin-converting enzyme (ACE) inhibitors and B-blockers would be the best possible treatment options [ 17 , 20 ]. Antioxidant supplements were also considered a great measure to reduce free radicals and oxidative stress, resulting from excessive training, therefore maintaining vascular endothelial health and function [ 21 ].…”