Abstract

We previously demonstrated that exogenous L‐Arg restores the blunted pressure diuresis and natriuresis relationship and normalizes arterial blood pressure in AngII‐infused rats. The present study determined the role of L‐Arg to modulate total renal blood flow and renal cortical and medullary blood flow in anesthetized, AngII‐infused, Sprague‐Dawley rats (n>6/group). Renal blood flow was measured by ultrasonic flowmetry and regional renal blood flow was evaluated with the use of implanted optical fibers for laser‐Doppler flowmetry. Aortic clamps were utilized to maintain renal perfusion pressure at 110 mmHg throughout the experiments. Intravenous infusion of AngII (20 ng/kg/min) resulted in a significant decrease in total renal blood flow from 7.2 ± 0.5 ml/min/gkwt to 5.3 ± 0.3 ml/min/gkwt. The AngII infusion did not significantly alter superficial cortical blood flow but significantly decreased medullary blood flow by 19 ± 4%. Co‐infusion of L‐Arg (300 μg/kg/min) reversed the effects of AngII to decrease renal blood flow and renal medullary perfusion. The present data demonstrate that AngII‐mediated vasoconstriction of the renal cortical and medullary vasculature is reversed by exogenous L‐Arg; these experiments indicate an important role for nitric oxide to blunt the renal vasoconstrictor, anti‐diuretic, and pro‐hypertensive effects of AngII. Supported by HL29587 and DK062803.

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