Microperfusion studies were conducted to determine if increases in distal nephron perfusion rate could lead to feedback-mediated decreases in stop-flow pressure (SFP) during autoregulatory-induced reductions in whole kidney vascular resistance. In the first group, renal arterial pressure (RAP) was reduced from 128 ± 2.6 to 91 ± 1.9 mmHg (SE), and in the second group renal venous pressure was elevated to 24 ± 29 mmHg. In both groups, significant reductions in whole kidney vascular resistance occurred, whereas renal blood flow remained unchanged. For the microperfusion procedure, a wax block was placed in the intermediate segment of the tubule and SFP was measured from an early tubule segment. Perfusion with an artificial tubule fluid solution was initiated in a terminal segment at a low perfusion rate (PR) of 16 nl/min and then increased to a high PR of 68 nl/min. In the first group, at control RAP (27 tubules) SFP was 57 ± 1.0 mmHg at low PR and then decreased to 33 ± 1.3 mmHg at high PR. At the reduced RAP (25 tubules), SFP was 43 ± 1.2 mmHg at low PR and decreased significantly to 31 ± 1.6 mmHg at the high PR. In the second group, at control venous pressure (17 tubules) SFP was 54 ± 1.4 mmHg at low PR and decreased to 28 ± 1.3 mmHg at high PR. With elevations in renal venous pressure (13 tubules), SFP was 55 ± 1.8 mmHg at low PR and decreased to 30 ± 2.1 mmHg at high PR. Accordingly, feedback responses during elevations in renal venous pressure were nearly identical to control values, thereby suggesting that the responsiveness of the feedback mechanism was unaltered during decreased renal vascular resistance. Also, significant feedback responses were still present when RAP was reduced, indicating that tubuloglomerular feedback can be elicited in the presence of autoregulatory-induced decreases in vascular resistance.