Autoregulation of renal blood flow. Effects of indomethacin and ureteral pressure

We tested the hypothesis that there is a common prostaglandin mediated stimulus to arteriolar vasodilation in response to elevated ureteral pressure and reduced arterial perfusion pressure. The responses of renal blood flow (RBF) to reduced renal artery pressure (RAP), elevated ureteral pressure (UP), and reduced RAP superimposed on UP were studied in untreated and indomethacin (I)-treated anesthetized dogs. In untreated dogs, the RBF response was variable, with increases, decreases, or no changes in RBF during reductions in RAP. In contrast, RBF was not increased in any of the I-treated dogs during reduction in RAP, but otherwise the responses were similar to untreated dogs. In the same dogs, RBF responses to elevated UP were evaluated at ureteral pressures of 20, 40, 60, and 80 mm Hg. In untreated dogs, RBF was significantly increased at all levels of elevated UP, while in I-treated dogs RBF did not change at 20, 40, and 60 mm Hg and decreased significantly at 80 mm Hg UP. The response of RBF to reduced RAP was studied in the presence of elevated UP. At 60 mm Hg ureteral pressure, autoregulation of RBF to reduced RAP was abolished in untreated dogs but did not change appreciably in I-treated dogs. We conclude that the renal vasodilation in response to elevated ureteral pressure is mediated by prostaglandins, while the response to reduced perfusion pressure is, for the most part, not mediated by prostaglandins.