Administration of exogenous L‐arginine (L‐Arg) attenuates angiotensin‐II (AngII)‐mediated hypertension and kidney disease in rats. The present study assessed renal hemodynamics and pressure diuresis–natriuresis in anaesthetized rats infused with vehicle, AngII (20 ng/kg per min i.v.) or AngII + L‐Arg (300 μg/kg per min i.v.). Experiments in isolated aortic rings were carried out to assess L‐Arg effects on the vasculature. Increasing renal perfusion pressure (RPP) from ˜100 to 140 mmHg resulted in a nine‐ to tenfold increase in urine flow and sodium excretion rate in control animals. In comparison, AngII infusion significantly reduced renal blood flow (RBF) and glomerular filtration rate (GFR) by 40–42%, and blunted the pressure‐dependent increase in urine flow and sodium excretion rate by 54–58% at elevated RPP. Supplementation of L‐Arg reversed the vasoconstrictor effects of AngII and restored pressure‐dependent diuresis to levels not significantly different from control rats. Dose‐dependent contraction to AngII (10−10 mol/L to 10−7 mol/L) was observed with a maximal force equal to 27 ± 3% of the response to 10−5 mol/L phenylephrine. Contraction to 10−7 mol/L AngII was blunted by 75 ± 3% with 10−4 mol/L L‐Arg. The influence of L‐Arg to blunt AngII‐mediated contraction was eliminated by endothelial denudation or incubation with nitric oxide synthase inhibitors. Furthermore, the addition of 10−3 mol/L cationic or neutral amino acids, which compete with L‐Arg for cellular uptake, blocked the effect of L‐Arg. Anionic amino acids did not influence the effects of L‐Arg on AngII‐mediated contraction. These studies show that L‐Arg blunts AngII‐mediated vascular contraction by an endothelial‐ and nitric oxide synthase‐dependent mechanism involving cellular uptake of L‐Arg.