NITRIC-OXIDE SYNTHESIS FROM L-ARGININE MODULATES RENAL VASCULAR-RESISTANCE IN ISOLATED PERFUSED AND INTACT RAT KIDNEYS

被引:42
作者
WELCH, WJ
WILCOX, CS
AISAKA, K
GROSS, SS
GRIFFITH, OW
FONTOURA, BMA
MAACK, T
LEVI, R
机构
[1] DEPT VET AFFAIRS MED CTR,NEPHROL & HYPERTENS SECT 111G,GAINESVILLE,FL 32608
[2] UNIV FLORIDA,DIV NEPHROL HYPERTENS & TRANSPLANTAT,GAINESVILLE,FL 32611
[3] CORNELL UNIV,MED CTR,COLL MED,DEPT PHARMACOL,NEW YORK,NY 10021
[4] CORNELL UNIV,MED CTR,COLL MED,DEPT BIOCHEM,NEW YORK,NY 10021
[5] CORNELL UNIV,MED CTR,COLL MED,DEPT PHYSIOL & BIOPHYS,NEW YORK,NY 10021
[6] CORNELL UNIV,MED CTR,COLL MED,CTR CARDIOVASC,NEW YORK,NY 10021
关键词
RAT KIDNEY; RENAL HEMODYNAMICS; L-NMA;
D O I
10.1097/00005344-199117003-00031
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This study tested the effects on renal hemodynamics of blockade of nitric oxide (NO) synthesis from L-arginine with N(G)-methyl-L-arginine (L-NMA) using both intact and isolated perfused rat kidneys. Infusion of L-NMA into anesthetized rats increased the mean arterial pressure and reduced the glomerular filtration rate and renal plasma flow only when the renal perfusion pressure was maintained at control levels. In isolated kidneys, L-NMA increased vascular resistance, this was attenuated by coadministration of L-arginine. L-NMA selectively inhibited acetylcholine-induced renal vasodilation without attenuating that elicited by sodium nitroprusside. We conclude that basal production of NO within both the intact and isolated kidney is required to maintain the normally high levels of renal blood flow and glomerular filtration and that endothelium-derived NO is an important regulator of renal vascular resistance.
引用
收藏
页码:S165 / S168
页数:4
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