We used a model of ischemic acute renal failure featuring normal renal blood flow (RBF) to evaluate the autoregulatory capability in a preparation having a marked reduction of inulin clearance (GFR). In 10 dogs, we clamped the renal artery for 90 min (experimental); 6 dogs, 1 min only (sham). Approximately 18 hours later, we determined the autoregulatory ability from RBF responses to renal arterial constriction. GFR of the experimental dogs was 10 ± 4 ml/min, significantly lower than GFR in the sham dogs (43 ± 9 ml/min). RBF in the experimental dogs (189 ± 17 ml/min) was not significantly different from that in the sham dogs (206 ± 32). An autoregulation index, ranging from 0.49 to 1.09 (mean 0.690), was significantly larger than was that of sham dogs, which ranged from zero to 0.23 (mean 0.060). At control arterial pressures, vascular resistance was comparable in both groups; however, at reduced arterial pressures below the normal autoregulatory range, average resistance of the experimental dogs (0.62 ± 0.12 mm Hg/[ml/min]) was significantly greater than was that of the sham dogs (0.38 ± 0.06 mm Hg/[ml/min]). These studies indicate that a substantial loss of renal hemodynamic responsiveness follows ischemic injury to the dog even when RBF is maintained within the normal range. The loss of autoregulatory capacity associated with a severely attenuated GFR is consistent with a role for tubular flow in the normal mechanism of autoregulation.