Effects of indomethacin on renal hemodynamic alterations caused by arterial and ureteral pressure changes in rabbits.

Abstract

Roles of prostaglandins in renal autoregulation and the distribution of cortical blood flow were studied in anesthetized rabbits, by means of prostaglandin synthesis inhibition. Within the range from 80 to 130mmHg in renal perfusion pressure, a constancy of renal blood flow was maintained. With an abrupt elevation of perfusion pressure from 100 to 130mmHg, blood flow did not alter in any regions of the cortex. In contrast, when perfusion pressure was reduced from 100 to 80mmHg, blood flow decreased in the outer cortex with reciprocal increase in the inner cortex. These hemodynamic changes were not affected by indomethacin. Acute ureteral pressure elevation to 50mmHg resulted in a redistribution of cortical flow to the inner cortex without significant change in renal blood flow. This redistribution was inhibited by indomethacin. During ureteral pressure elevation, autoregulation was impaired. In this situation, a rise of perfusion pressure produced a significant increase in blood flow in the outer cortex without significant change elsewhere. A reduction of perfusion pressure gave rise to significant decrease in flow in the outer cortex without an increase in the inner cortex. In indomethacin-treated rabbits, ureteral pressure elevation impaired autoregulation slightly but not significantly. These findings suggest 1) good autoregulatory capability in all regions of the renal cortex; and 2) a minor role of prostaglandins in the development of renal autoregulation in normal rabbits but a partial contribution to the impairment of autoregulation during ureteral pressure elevation.