RENAL VASODILATION WITH L-ARGININE - EFFECTS OF DIETARY SALT

Infusion of L-arginine, the substrate for nitric oxide synthase, cause s renal vasodilation. Since dietary salt restriction blunts the renal vasoconstrictor response to inhibition of nitric oxide synthase, we in vestigated the hypothesis that dietary salt intake determines the rena l vascular response to L-arginine. Bolus intravenous doses of L-argini ne given to anesthetized Sprague-Dawley rats caused dose-dependent inc reases 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. Comp ared with rats adapted to a high salt diet, those adapted to a low sal t diet were more sensitive to the reductions in blood pressure and ren al vascular resistance (threshold dose of L-arginine for renal Vascula r resistance: low salt, 2.9+/-0.9 mu mol . kg(-1) versus high salt, 20 .0+/-6.2; P<.025), but the maximal changes in renal vascular resistanc e 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 respon se 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 t he renal vasoconstrictor response to N-G-nitro-L-arginine methyl ester . In conclusion, renal vasodilation is more sensitive to L-arginine du ring salt restriction. This effect is specific for L-arginine. A decre ased 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.