Angiotensin-converting enzyme inhibition does not suppress plasma angiotensin II increase during exercise in humans.

Physical effort stimulates the reninangiotensin system (RAS). We studied the effect of an angiotensin-converting enzyme inhibitor (ACE inhibitor) in a double-blind placebo-controlled study, on eight volunteers undergoing physical stress on an ergometric bicycle. The effects of captopril (C) (50 mg, three times daily for 3 days) on arterial pressure (AP), O2 consumption (VO2), variations in auricular natriuretic factor (ANF), renin, angiotensin II (AII) plasma levels, as well as glomerular filtration rate (GFR) and microalbuminuria (MA) were evaluated. The different parameters were compared by analysis of variance (ANOVA). The pressure profile and VO2 were not modified by ACE inhibitor. Exercise stimulates release of renin; this action was greater with captopril administration (treatment effect: p < 10(-4), indicating blockade of the RAS. This inhibition was incomplete because AII levels increased markedly when captopril was given (no treatment effect: p < 0.37). Finally, ACE inhibitor resulted in decreased GFR (p = 115 +/- 5.8 ml/mn-1, C = 91.1 +/- 4, p < 0.05) with exercise without modification of MA. ACE inhibitor administration does not modify the physical performance of nonathletic subjects; AII is significantly increased with exercise despite captopril treatment; ACE inhibitor decreases GFR significantly but does not influence MA with prolonged physical effort.