Augmented pulmonary vascular and venous constrictions to N G-nitro-L-arginine methyl ester in rats with monocrotaline-induced pulmonary hypertension

Abstract

The hemodynamic effects of NG-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide (NO) synthase) were examined in thiobutabarbital-anesthetized control- rats and rats with monocrotaline-induced pulmonary hypertension. L-NAME (1-16 mg/kg i.v.) increased mean arterial pressure, systemic vascular resistance, venous resistance and pulmonary vascular resistance, and decreased cardiac output in both the control and pulmonary hypertensive rats. Relative to the controls, L-NAME (16 mg/kg) caused a smaller increase (≈50% of control) in mean arterial pressure in the pulmonary hypertensive rats, but greater increases in venous (≈200%) as well as pulmonary vascular (≈400%) resistances and a greater decrease in cardiac output (≈140%). The results show that NO is an important dilator within the arterial, venous and pulmonary circulation; its pulmonary and venous dilator roles are augmented in pulmonary hypertension. Copyright © 2003 S. Karger AG, Basel.