Renal blood flow and vasodilatory ability prior to and following release of 24 hours bilateral ureteral obstruction in rats.

Increased renal vascular resistance (RVR) is evident after 24 hours of uni- and bilateral ureteral obstruction (UUO and BUO). However, to what extent the RVR increase is due to vascular damage versus functional vasoconstriction, or whether obstructed kidneys possess the ability to reduce RVR in response to vasodilatory stimuli, is not clear. During 24 hours of BUO renal blood flow (RBF), recorded electromagnetically, was reduced to about 70% of control and continued to fall by another 18% during 1/2-1 hour after release of BUO. Infusion of imidazole, a thromboxane A2 synthetase blocker, did not reduce RVR after release of BUO. Whereas RBF autoregulation in response to reduced perfusion pressure was impaired, maximal proportional renal vasodilation induced by acetylcholine was increased, both prior to and after release of BUO, as compared to control and UUO. These different renal vasodilatory responses indicate that the RVR increase during BUO is largely due to a functional vasoconstriction that impairs autoregulatory vasodilation. In contrast, the RVR increase during UUO is probably mainly due to structural damage which does not prevent autoregulation of the RBF level attained.