Effect of systemic nitric oxide synthase inhibition on postexercise hypotension in humans

An acute bout of aerobic exercise results in a reduced blood pressure that lasts several hours. Animal studies suggest this response is mediated by in creased production of nitric oxide. We tested the extent to which systemic nitric oxide synthase inhibition [N-G-monomethyl-L-arginine (L-NMM] can rev erse the drop in blood pressure that occurs alter exercise in humans. Eight healthy subjects underwent parallel experiments on 2 separate days. The or der of the experiments was randomized between sham (60 min of seated uprigh t rest) and exercise (60 min of upright cycling at 60% peak aerobic capacit y). After both sham and exercise, subjects received, in sequence, systemic alpha -adrenergic blockade (phentolamine) and L-NMMA. Phentolamine was give n first to isolate the contribution of nitric oxide to postexercise hypoten sion by preventing reflex changes in sympathetic tone that result from syst emic nitric oxide synthase inhibition and to control for alterations in res ting sympathetic activity after exercise. During each condition, systemic a nd regional hemodynamics were measured. Throughout the study, arterial pres sure and vascular resistances remained lower postexercise vs. postsham desp ite nitric oxide synthase inhibition (e.g., mean arterial pressure after L- NMMA was 108.0 +/- 2.4 mmHg postsham vs. 102.1 +/- 3.3 mmHg postexercise; P < 0.05). Thus it does not appear that postexercise hypotension is dependen t on increased production of nitric oxide in humans.