Role of nitric oxide in the vasodilator response to mental stress in normal subjects

Abstract

Vascular production of nitric oxide (NO) plays an important role in a variety of physiologic processes. This study examines the contribution of NO to the vasodilator response to mental stress. The effects of mental arithmetic testing on forearm vascular dynamics were analyzed in 15 normal subjects (9 men; age 45 ± 12 years) during intraarterial infusion of either saline or N G-monomethyl- l-arginine ( l-NMMA; 4 μmol/min for 15 minutes), an inhibitor of NO synthesis. The effect of l-NMMA on endothelium-independent vasodilation induced by intraarterial infusion of sodium nitroprusside was also studied in 11 of the 15 subjects. Forearm blood flow was measured by plethysmography. Mental stress increased forearm blood flow from 2.35 ± 0.84 to 5.06 ± 2.66 ml/min/dl (115%) during saline and from 1.72 ± 0.59 to 2.81 ± 0.99 ml/min/dl (63%) during l-NMMA infusion. The vasodilator effect of mental stress was significantly lower during l-NMMA infusion than during saline (1.1 ± 0.65 vs 2.71 ± 2.15 ml/min/dl; p = 0.01). l-NMMA administration did not significantly change mean arterial pressure and heart rate responses to mental stress. In contrast, the vasodilator effect of sodium nitroprusside (1.6 μg/min) was similar during infusion of l-NMMA and during saline (3.75 ± 1.55 vs 2.85 ± 1.38 ml/min/dl; p = 0.16). These findings indicate that local release of NO is involved in the forearm vasodilator response to mental stress.