EFFECTS OF NITRIC-OXIDE INHIBITION ON SYSTEMIC AND RENAL HEMODYNAMICSIN THE HEMORRHAGED RAT

The systemic and renal hemodynamic responses to nitric oxide (NO) inhi bition with L-Name were compared in both normotensive, normovolemic ra ts and in rats following acute hemorrhagic hypotension. The mean arter ial 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+/ -19%) than in hypotensive rats (64+/-14%). The renal vascular resistan ce also increased more in normotensive rats (189+/-20%) than in hypote nsive rats (102+/-19%; p<0.05). The glomerular filtration rate was mar kedly 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-ind uced increase in vascular resistance is markedly reduced following hem orrhage, suggesting that NO production or availability is reduced. How ever, the NO production continues in the hemorrhaged rat and contribut es substantially to the hypotension and functional renal insufficiency associated with acute severe volume depletion.