Shear-induced modulation by nitric oxide of sympathetic nerves in the superior mesenteric artery

We tested the hypothesis that nerve-induced constriction is modulated by nitric oxide only if shear stress is allowed to increase. Shear stress is the effect of moving fluid producing distortion of endothelial cells. Blood flow to the superior mesenteric artery in anesthetized cats was controlled using a perfusion circuit. Shear stress was increased by holding blood flow constant during vasoconstriction induced by nerve stimulation (2 and 10 Hz) or infusion of norepinephrine (0.5 microgram.kg-1.min-1). The increase in perfusion pressure in response to nerve stimulation when shear stress was allowed to rise was 24.8 +/- 4.7 mmHg (1 mmHg = 133.3 Pa) (2 Hz) and 100.0 +/- 17.8 mmHg (10 Hz). After NO synthase blockade using NG-nitro-L-arginine methyl ester (L-NAME) (2.5 mg/kg i.v.) potentiation occurred (74.0 +/- 21.6 mmHg at 2 Hz and 151.9 +/- 14.1 mmHg at 10 Hz). Potentiation was reversed after L-arginine (75 mg/kg i.v.). When shear stress was held constant, L-NAME did not affect the responses to nerve stimulation. In contrast, the vasoconstriction to norepinephrine was not affected by L-NAME. The data are compatible with the hypothesis that if vasoconstriction leads to increased shear stress, release of nitric oxide produces vasodilation subsequent to decreased sympathetic nerve activity. The absence of a similar effect with norepinephrine suggests that the shear-dependent release of nitric oxide at the site of constriction does not act directly on the vascular smooth muscle in the small resistance vessels.