Our earlier studies have shown development of endothelial dysfunction in the feline renal artery during hemorrhagic hypotension. Because L-arginine (L-Arg), the precursor of nitric oxide (NO), reportedly improves endothelial function in several pathophysiological states including hypotension, we investigated its possible beneficial effect on the adrenal and renal circulations during hemorrhagic hypotension in anesthetized, ventilated cats. Hypotension (mean arterial pressure 50 mm Hg) significantly increased vascular resistance and decreased blood flow (radiolabeled microspheres) in both adrenal and renal cortices. L-Arg (30 mg/kg bolus, 10 mg/kg/min infusion, i.v.) had no significant hemodynamic effects in normotension but prevented the increase of the vascular resistance and improved blood flow in the adrenal cortex during hypotension. In the kidney, L-Arg also prevented hemorrhage-induced vasoconstriction, although its effect on blood flow did not reach significance. The NO synthase inhibitor N(G)-nitro-L-arginine (30 mg/kg bolus, 1 mg/kg/min infusion, i.v.) increased adrenal and renal vascular resistances to a similar extent as that observed during hypotension. It thus seems that an L-Arg-reversible dysfunction of the endothelial NO-synthesizing pathway contributes to hemorrhage-induced adrenal and renal vasoconstriction.