Renal Effects of Acute Amino Acid Infusion in Hypertension Induced by Chronic Nitric Oxide Blockade

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Abstract
L -Arginine is the physiological substrate of nitric oxide, a vasodilator that controls blood pressure and renal hemodynamics in the basal state. In the present studies, we produced chronic nitric oxide blockade by oral administration of the l -arginine analogue N G -nitro- l -arginine methyl ester, which produced sustained hypertension and increased renal vascular resistance in conscious rats. Acute excess l -arginine had little effect on blood pressure but completely normalized renal vascular resistance and increased renal plasma flow in chronically nitric oxide–blocked hypertensive rats. In contrast to l -arginine, d -arginine had no renal hemodynamic effects in either normal or chronically nitric oxide–blocked rats. Acutely administered glycine was ineffective in vasodilating the chronically nitric oxide–blocked rat kidney, in a dose that produced renal vasodilation in normal rats. These findings indicate the following: (1) Hypertension induced by chronic nitric oxide blockade due to substituted l -arginine analogue cannot be acutely reversed with excess L-arginine, suggesting that the maintenance of the hypertension is not solely caused by competitive inhibition of nitric oxide production; (2) in contrast, the kidney remains responsive to l -arginine whereas the renal vasodilator response to glycine is abolished in this model of hypertension.