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Captopril does not Potentiate Post-Exercise Hypotension: A Randomized Crossover Study
Andréia Cristiane Carrenho Queiroz1, Julio Cesar Silva Sousa1, Natan Daniel Silva1
1School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil.
Insights
Captopril did not enhance post-resistance exercise hypotension (PREH) in hypertensive men. This study found no significant differences in blood pressure reduction or underlying mechanisms between captopril and placebo treatments after exercise.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Pharmacology
Background:
- Hypertension (HT) management often involves medication.
- Post-resistance exercise hypotension (PREH) is a phenomenon where blood pressure decreases after resistance exercise.
- The potential potentiation of PREH by antihypertensive medications requires investigation.
Purpose of the Study:
- To determine if captopril potentiates post-resistance exercise hypotension (PREH) in hypertensive men.
- To investigate the effects of captopril on the characteristics and mechanisms of PREH.
- To compare PREH following resistance exercise with captopril versus placebo.
Main Methods:
- A double-blinded, randomized-crossover study involving 12 hypertensive men.
- Subjects received captopril (3x50 mg/day) and placebo for 4 weeks each.
- Blood pressure and hemodynamic variables were measured during control and resistance exercise sessions, with 24-hour ambulatory monitoring.
Main Results:
- Captopril did not alter the magnitude or duration of post-resistance exercise hypotension compared to placebo.
- Systolic and diastolic blood pressure decreased similarly after resistance exercise in both treatment periods.
- No significant differences were observed in the hemodynamic mechanisms underlying PREH between captopril and placebo conditions.
Conclusions:
- Captopril does not potentiate post-resistance exercise hypotension in hypertensive men.
- The antihypertensive medication captopril does not influence the mechanisms or extent of PREH.
- Resistance exercise elicits hypotension independently of captopril treatment in this population.
Abstract:
To evaluate whether captopril (3×50 mg/day) potentiates post-resistance exercise hypotension (PREH) in hypertensives (HT), 12 HT men received captopril and placebo for 4 weeks each in a double-blinded, randomized-crossover design. On each therapy, subjects underwent 2 sessions: Control (C - rest) and Resistance Exercise (RE - 7 exercises, 3 sets to moderate fatigue, 50% of 1 RM -repetition maximum). Measurements were taken before and after 30-60 min (Post1) and 7 h (Post2), and ambulatory blood pressure (BP) was monitored for 24 h. There were no differences in PREH characteristics and mechanisms between the placebo and captopril periods. At Post1, systolic/diastolic BP decreased significantly and similarly after RE with both therapies (Placebo=-13±2/-9±1 mmHg vs. Captopril=-12±2/-10±1 mmHg, P<0.05). RE reduced cardiac output in some subjects and systemic vascular resistance in others. Heart rate and cardiac sympathetic modulation increased, while stroke volume and baroreflex sensitivity decreased after RE (Placebo: +13±2 bpm, +21±5 nu, -11±5 ml, -4±2 ms/mmHg; Captopril: +13±2 bpm, +35±4 nu, 17±5 ml, -3±1 ms/mmHg, P<0.05). At Post2, all variables returned to pre-intervention values. Ambulatory BP was similar between the sessions. Thus, captopril did not potentiate the magnitude and duration of PREH in HT men, and it did not influence PREH mechanisms.
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