A Central Pressor Response to Endogenous Nitric Oxide Synthesis Inhibition in Anesthetized Rats

A Central Pressor Response to Endogenous Nitric Oxide Synthesis Inhibition in Anesthetized Rats

The present study was aimed to determine if endogenous L-arginine-nitric oxide (NO) pathway has central, rather than peripheral, mechanisms in blood pressure regulation. Arterial blood pressure and heart rate responses to acute inhibition of the t-arginine-NO pathway were examined in rats anesthetized with thiopental (50 mg/kg, IP). An intracerebroventricular (ICV) cannula was placed in the left lateral ventricle. The right femoral artery was cannulated to measure arterial blood pressure and the vein to serve as an infusion route. N^G-nitro-L-arginine methyl ester (L-NAME) was infused either intracerebroventricularly or intravenously. ICV infusion (1.25 μL/min) of L-NAME (20 or 100 μg/kg) per minute for 60 min) increased the mean arterial pressure and heart rate. Plasma renin concentrations(PRC) were significantly lower in L-NAME-infused group than in the control. L-Arginine (60 μg/min, ICV) prevented the pressor response to ICV L-NAME. The pressor response was not affected by simultaneous intravenous infusion of saralasin, but was abolished by hexamethonium treatment. Intravenous infusion (40 μL/min, 10 ~ 100 μg/kg per minute for 60 min) also increased blood pressure, while it decreased heart rate. These results indicate that endogenous L-arginine-NO pathway has separate central and peripheral mechanisms in regulating the cardiovascular function. The central effect may not be mediated via activation of renin-angiotensin system, but via, at least in part, activation of the sympathetic outflow.