Cortisol inhibits cholinergic vasodilatation in the human forearm

dExogenous cortisol raises blood pressure (BP) in humans and there is accum ulating evidence of abnormalities of glucocorticoid activity in essential h ypertension. In this study we tested the hypothesis that exogenous cortisol attenuates the cholinergic dilator response in the forearm circulation. Fo urteen healthy normotensive men were studied. Using bilateral forearm venou s plethysmography, we examined forearm blood now responses to intra-arteria l acetylcholine (ACh) and sodium nitroprusside (SNP) pre- and post-N-G-mono methyl-L-arginine (LNMMA)after 2 or 5 days of oral cortisol or placebo in a randomized, double-blind crossover study. Exogenous cortisol increased supine systolic (P < .05) and standing systoli c (P < .05) BP and produced expected metabolic changes and suppressed serum cortisol concentration (P < .001). Baseline forearm blood now did not diff er between placebo and cortisol treatments at 2 or 5 days. Cholinergic vaso dilatation was impaired after cortisol administration, reaching statistical significance at 5 days (P < .05), Cortisol did not affect responses to SNP . N-G-monomethyl-L-arginine inhibited cholinergic vasodilatation in placebo -treated groups but had no additional effect in the presence of cortisol. These results support our hypothesis and suggest that the mechanism of impa ired cholinergic dilatation in glucocorticoid-treated subjects involves abn ormalities of the endothelial nitric oxide system. Am J Hypertens 2000; 13: 1155-1160 (C) 2000 American Journal of Hypertension, Ltd.