SYSTEMIC AND REGIONAL HEMODYNAMICS AFTER NITRIC-OXIDE SYNTHASE INHIBITION ROLE OF A NEUROGENIC MECHANISM

The study tested the hypothesis that the increase in blood pressure an d decrease in cardiac output after nitric oxide (NO) synthase inhibiti on with N-omega-nitro-L-arginine methyl ester (L-NAME) was partially m ediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive mi crospheres. All measurements of pressure and flows were made before an d after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervo us system was blocked by 20 mg/kg hexamethonium. In this group of anim als, an intravenous infusion of norepinephrine (20-140 ng/min) was use d to maintain normal blood pressure. L-NAME treatment resulted in a si gnificant increase in mean arterial pressure in both groups. L-NAME tr eatment decreased cardiac output similar to 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decreas e in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in bl ood pressure and decreases in cardiac output and tissue flows after L- NAME treatment are not dependent on a neurogenic mechanism.