Renal Vasodilation With l -Arginine

Abstract

Abstract Infusion of l -arginine, the substrate for nitric oxide synthase, causes renal vasodilation. Since dietary salt restriction blunts the renal vasoconstrictor response to inhibition of nitric oxide synthase, we investigated the hypothesis that dietary salt intake determines the renal vascular response to l -arginine. Bolus intravenous doses of l -arginine given to anesthetized Sprague-Dawley rats caused dose-dependent increases in renal blood flow and decreases in renal vascular resistance, whereas d -arginine was not effective. The response to l -arginine was prevented by pretreatment with N G -nitro- l -arginine methyl ester. Compared with rats adapted to a high salt diet, those adapted to a low salt diet were more sensitive to the reductions in blood pressure and renal vascular resistance (threshold dose of l -arginine for renal vascular resistance: low salt, 2.9±0.9 μmol · kg −1 versus high salt, 20.0±6.2; P <.025), but the maximal changes in renal vascular resistance were similar (low salt, −43±5% versus high salt, −34±5%; P =NS). Bolus doses of l -glycine also caused dose-dependent renal vasodilation, but the renal vasodilator responses were not affected by salt intake. Preinfusion of l -arginine augmented the renal vasoconstrictor response to N G -nitro- l -arginine methyl ester in low salt but not high salt rats; after l -arginine dietary salt no longer significantly affected the renal vasoconstrictor response to N G -nitro- l -arginine methyl ester. In conclusion, renal vasodilation is more sensitive to l -arginine during salt restriction. This effect is specific for l -arginine. A decreased availability of l -arginine during low salt intake may limit renal nitric oxide generation and thereby reduce the renal vasoconstrictor response to inhibition of nitric oxide synthase.