ABSTRACT
The increase in ureteral pressure after acute unilateral ureteral obstruction (UUO) is associated with an initial increase in renal blood flow (RBF). The present study examines the role of nitric oxide, a major endothelium-derived relaxing factor (EDRF), in UUO-induced renal hyperemia in anesthetized dogs. In Group 1, vehicle solution was infused into the left renal artery. In Group 2, nitric oxide formation from L-arginine was competitively inhibited by intrarenal infusion of N omega-monomethyl-L-arginine (L-NMMA) (50 micrograms/kg./min.) before UUO. In Group 3, L-arginine (2 mg./kg./min.) was infused together with L-NMMA (50 micrograms/kg./min.) into the renal artery. After UUO, ureteral pressure increased in all groups, averaging 69 mm.Hg. In Group 1, RBF at 10 and 20 minutes after UUO increased 7.9 +/- 1.6% and 16.5 +/- 5.2%, respectively, significantly greater than in Group 2 (1.2 +/- 1.6% and 2.4 +/- 1.5%). After L-NMMA was discontinued in Group 2, RBF increased 17%, reaching a level similar to that in Group 1. In Group 3, L-arginine infusion abolished the effects of L-NMMA, and RBF was similar to that in Group 1 at all postobstructive intervals. Our data indicate that release of nitric oxide in the kidney is augmented by UUO and mediates the early renal hyperemia induced by UUO.
