The systemic and renal hemodynamic responses to nitric oxide (NO) inhibition with L-Name were compared in both normotensive, normovolemic rats and in rats following acute hemorrhagic hypotension. The mean arterial blood pressure increased in normovolemic as well as in hemorrhaged, hypotensive rats. The systemic vascular resistance also increased in both groups, but the increase was greater in normotensive rats (104 +/- 11%) than in hypotensive rats (64 +/- 14%). The renal vascular resistance also increased more in normotensive rats (189 +/- 20%) than in hypotensive rats (102 +/- 19%; p < 0.05). The glomerular filtration rate was markedly reduced by L-Name in normovolemic rats (from 3.0 +/- 0.1 to 2.1 +/- 0.1 ml/min/300 g), but increased in hemorrhaged rats following L-Name (from 1.8 +/- 0.2 to 2.5 +/- 0.2 ml/min/300 g). In summary, the L-Name-induced increase in vascular resistance is markedly reduced following hemorrhage, suggesting that NO production or availability is reduced. However, the NO production continues in the hemorrhaged rat and contributes substantially to the hypotension and functional renal insufficiency associated with acute severe volume depletion.