This study was conducted on anesthetized dogs utilizing an electromagnetic flowmeter probe around the renal artery and inulin extraction ratios for the calculation of glomerular filtration rate. At maximal ureteral pressures, renal blood flow increased to almost twice the control values. Glomerular filtration rate increased slightly, but significantly, with small elevations in ureteral pressure and returned, with further elevations, to values not significantly different from control. Renal arterial pressure-blood flow relationships demonstrated that autoregulatory capacity was diminished with ureteral pressure elevation, and a nearly passive behavior was observed at maximal ureteral pressures. Urine flow progressively decreased as the ureteral pressure was elevated and approximately half of the dogs could not generate ureteral pressures above 60 mm Hg. Sodium and chloride excretion rates decreased to a greater, potassium to a lesser, and osmolal excretion rates to the same extent as urine flow. Upon return to zero ureteral pressure, polyuria was observed although the sodium, chloride, and osmolal excretion rates were not significantly different from control values. RBF and GFR also returned to control levels and autoregulatory capacity was re-established. The results are interpreted to indicate that elevation of ureteral pressure results in a reversible decrease in vascular resistance at preglomerular sites through some feedback mechanism which may involve factors within the tubular network.