RACIAL-DIFFERENCES IN NITRIC OXIDE-MEDIATED VASODILATOR RESPONSE TO MENTAL STRESS IN THE FOREARM CIRCULATION

An abnormal hemodynamic response to stressful stimuli has been propose d as a mechanism involved in the higher prevalence of hypertension in blacks. Given the important role of nitric oxide (NO) in the regulatio n of cardiovascular homeostasis, we investigated the possibility of ra cial differences in vascular NO activity during mental stress. To test this hypothesis, we compared the forearm blood flow (FBF) response to mental stress in 14 white and 12 black healthy subjects during intra- arterial infusion of either saline or NO synthesis inhibitor N-G-monom ethyl-L-arginine (L-NMMA; 4 mu mol/min). We also examined vascular res ponses of the two groups to intra-arterial infusion of sodium nitropru sside (0.8 to 3.2 mu g/min), an exogenous NO donor. During saline infu sion, the increase in FBF from baseline induced by mental stress was s ignificantly higher in whites than in blacks (109+/-20% versus 58+/-8% ; P=0.03). L-NMMA significantly reduced stress-induced increase in FBF in whites (from 109+/-20% to 54+/-11%; P=0.004) but not in blacks (fr om 58+/-8% to 42+/-10%; P=0.24); thus, the vasodilator effect of stres s testing during L-NMMA was similar in whites and blacks (54+/-11% ver sus 42+/-10%; P=0.44). The vasodilator response to sodium nitroprussid e was also lower in blacks than in whites (maximum flow, 6.9+/-2 versu s 11.6+/-3.5 mL.min(-)1.dL(-1); P=0.001) and was not significantly mod ified by L-NMMA in either group. Our findings indicate that blacks hav e a reduced NO-dependent vasodilator activity during mental stress. Th is difference seems related to reduced sensitivity of smooth muscle to the vasodilator effect of NO and may play some role in the increased prevalence of hypertension and its complications in blacks.