In order to evaluate vascular (myogenic) and tubular (tubuloglomerular feedback) mechanisms involved in renal blood flow (RBF) autoregulation, canine kidneys with filtration (normal) and without filtration (nonfiltering, NFK; ureteral-obstructed, UO) were studied. RBF was monitored in response to stepwise reductions in renal perfusion pressure of –20, –40, and –60 mm Hg from control pressure. None of the three groups demonstrated significant changes in RBF from their respective control values (normal, 380 ml/min/100 g; NFK, 179 ml/min/100 g; UO, 153 ml/min/100 g) until the lowest pressure (–60 mm Hg from control pressure). All three groups responded to the pressure reductions with significant decreases in renal vascular resistance. However, the calculated efficiency of the autoregulatory response for the NFK and UO groups was significantly less than for the normal group. Elimination of tubuloglomerular feedback (NFK and UO) did not necessarily eliminate renal vascular autoregulation, but did reduce the efficiency of autoregulation. It is suggested that both vascular (myogenic) and tubular (tubuloglomerular) mechanisms may coexist to efficiently autoregulate blood flow in normal filtering kidneys. However, a reduction in metabolic activity as a contributor to the reduced ability to autoregulate in these kidneys could be an additional possibility.