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Exogenous L‐Arginine (L‐Arg) blunts Angiotensin II (AngII)‐mediated renal vasoconstriction and improves pressure‐diuresis

Administration of exogenous L‐Arg reverses AngII‐mediated hypertension and kidney disease in conscious rats. The present study assessed renal hemodynamics and pressure‐diuresis in Inactin‐anesthetized Sprague Dawley rats (n=4‐5/group) infused with saline vehicle, AngII (20 ng/kg/min, iv) or AngII + L‐Arg (300 ?g/kg/min, iv). Increasing renal perfusion pressure (RPP) from 100±1 to 142±3 mmHg with aortic clamps resulted in an increase in urine flow in control rats from 5.3±0.6 to 56.1±12.5 ?l/min/gram kidney weight (gkwt). In comparison, the pressure‐dependent increase in urine flow was significantly depressed by 50‐65% at all levels of RPP in AngII‐infused rats. Supplementation of L‐Arg restored pressure‐dependent diuresis to levels not significantly different from control rats. In control rats, glomerular filtration rate (GFR) averaged 1.4±0.4 ml/min/gkwt and renal blood flow (RBF) averaged 6.8±0.7 ml/min/gkwt at the lowest RPP. RBF was significantly reduced by 45% in AngII‐infused rats. Co‐infusion of L‐Arg reversed the AngII‐mediated changes in RBF to values not different from control. These data indicate that AngII‐mediated vasoconstriction and blunting of pressure‐diuresis is reversed by exogenous L‐Arg, demonstrating an important role for nitric oxide to blunt the renal vasoconstrictor, anti‐diuretic, and pro‐hypertensive effects of AngII. Supported by DK‐62803.