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Basal and hormone-stimulated prostaglandin biosynthesis was compared in isolated perfused rabbit kidneys with and without ureteral obstruction. At 72 h there was enhanced responsiveness to bradykinin in the ureter-obstructed hydronephrotic kidney. The amount of prostaglandin-like substance released from the perfused kidneys by 25 ng of bradykinin was 533+/-163 ng from the ureter-obstructed, 28+/-4 ng from the contralateral, and 26+/-3 ng from the normal kidney. The enhanced response was also noted with angiotensin II and with norepinephrine. This exaggerated responsiveness by the ureter-obstructed kidney could not be explained by decreased prostaglandin (PG) destruction or by decreased renal peptide inactivation (bradykinin or angiotensin). There was no enhanced PG biosynthesis with exogenous arachidonate, suggesting there was no increase in cyclo-oxygenase activity in the ureter-obstructed kidney. Renal tubular transport of PG from medulla to cortex was apparently not essential for the enhanced PG biosynthesis to hormone stimulation since the same exaggerated responses were noted during perfusion with the ureter ligated. The cyclo-oxygenase inhibitor, indomethacin, increased basal perfusion pressure in the obstructed kidney and enhanced the magnitude and duration of the renal vasoconstriction produced by angiotensin II in the hydronephrotic kidney. These results suggest that the local exaggerated biosynthesis of PG may be occurring in the cortical resistance vessels and may be important to the alteration in blood flow and excretory function that occur in ureteral obstruction.

Exaggerated prostaglandin biosynthesis and its influence on renal resistance in the isolated hydronephrotic rabbit kidney.