Abstract

The effects of indomethacin (INDO) and imidazole (IMID) on postobstructed kidney functions were evaluated in dogs after 24 h of bilateral ureteral obstruction (BUO). In vehicle-treated dogs 1 h after release of BUO, clearances of inulin and PAH (Cin and Cpah) were 37 and 26%, respectively, of the preobstruction values. Fractional sodium excretion (FEna) increased from 0.5 +/- 0.1 to 2.9 +/- 0.6. Urine osmolality (Uosmol) increased by 55 +/- 9 mosmol/kg H2O in response to 50 mU of aqueous vasopressin. In INDO-treated dogs, Cin and Cpah were 39 and 21%, respectively, of the preobstruction values. FEna increased from 0.7 +/- 0.2 to 4.0 +/- 0.9. Uosmol increased by 91 +/- 19 mosmol/kg H2O in response to vasopressin. This lack of beneficial effects of INDO may reflect its cancelling effect on prostaglandins' and thromboxanes' (TX) effects on the renal hemodynamics of the postobstructed kidney. To further assess the roles of TX in the postobstructed kidney, IMID, and inhibitor of TX synthesis, was given before the release of obstruction. In this group of dogs, the Cin of the postobstructed kidney did not differ from the preobstruction value. CC pah was 45% of the preobstruction value, a level significantly higher than in either vehicle- or INDO-treated dogs. FEna wa 1.5 +/- 0.2 before and 3.5 +/- 2.3 after obstruction. Uosmol increased by 187 +/- 51 mosmol/kg H2O after vasopressin, a level significantly higher than in vehicle-treated dogs. The present study suggests that IMID improves Cin, Cpah, FEna, and concentrating ability of the postobstructed kidney. TX may be responsible for the persistent reductions of Cin and Cpah in the postobstructed kidney.

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