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(Hypertension. 1995;25:61-66.)
© 1995 American Heart Association, Inc.

Articles

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

Changbin Qiu; Kevin Engels; Lennie Samsell; Chris Baylis

From the Department of Physiology, Robert C. Byrd Health Sciences Center of West Virginia University, Morgantown.

Correspondence to Changbin Qiu, MD, Department of Physiology, Robert C. Byrd Health Sciences Center of West Virginia University, PO Box 9229, Morgantown, WV 26506-9229.

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.

Key Words: rats • nitric oxide • vascular resistance • vasodilation • hypertension, chronic • arginine • glycine

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