C. Cardillo et al., RACIAL-DIFFERENCES IN NITRIC OXIDE-MEDIATED VASODILATOR RESPONSE TO MENTAL STRESS IN THE FOREARM CIRCULATION, Hypertension, 31(6), 1998, pp. 1235-1239
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.