Augmented pulmonary vascular and venous constrictions to N(G)-nitro-L-arginine methyl ester in rats with monocrotaline-induced pulmonary hypertension.
The hemodynamic effects of N(G)-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 (approximately 50% of control) in mean arterial pressure in the pulmonary hypertensive rats, but greater increases in venous (approximately 200%) as well as pulmonary vascular (approximately 400%) resistances and a greater decrease in cardiac output (approximately 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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D016686:Monocrotaline; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
D009569:Nitric Oxide; D016686:Monocrotaline; D019331:NG-Nitroarginine Methyl Ester