Attenuated central pressor response to nitric oxide synthesis inhibition in chronic renal failure rats.

Abstract

ObjectivesCentral and peripheral roles of nitric oxide (NO) in blood pressure regulation have been suggested. The present study was aimed at examining if the role of NO in blood pressure regulation is altered in chronic renal failure.MethodsBlood pressure responses to acute inhibition of NO were examined in 5/6 nephrectomized rats. Three weeks after the renal ablation, under thiopental (50 mg/kg, i.p.) anesthesia, an intracerebroventricuiar cannula was placed in the left lateral ventricle and the femoral vein was cannuiated to serve as an infusion route. The arterial blood pressure was measured in the right femoral artery. NG-nito-L-arginine methyl ester (L-NAME) was infused (100μg/kg per min for 60 min) either intracerebroventricularly or intravenously.ResultsChronic renal failure rats showed a significantly higher arterial pressure than the control rats (147±14mmHg vs. 122±13mmHg). Intracerebroventricuiar L-NAME did not affect the arterial pressure in chronic renal failure rats (0.5±4mmHg increase from the basal), while it significantly increased the arterial pressure in normal rats (22±3mmHg increases from the basal). Intravenous L-NAME increased the arterial pressure, the magnitude of which did not differ between the normal and chronic renal failure rats (24±3 vs. 16±3mmHg increases from the basal).ConclusionThese results indicate that the central role of NO in the regulation of blood pressure is altered in chronic renal failure.