Renal Effects of Acute Amino Acid Infusion in Hypertension Induced by Chronic Nitric Oxide Blockade
作者:
Changbin Qiu,
Kevin Engels,
Lennie Samsell,
Chris Baylis,
期刊:
Hypertension
(OVID Available online 1995)
卷期:
Volume 25,
issue 1
页码: 61-66
ISSN:0194-911X
年代: 1995
出版商: OVID
数据来源: OVID
摘要:
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 NG-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. (Hypertension. 1995;25:61-66.)
返 回