1. The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF). 2. The transfer function between 0.0018 and 0.5 Hz was calculated from the spontaneous fluctuations in renal arterial blood pressure (RABP) and renal blood flow (RBF) in conscious resting dogs. The response of RBF to stepwise artificially induced reductions in RABP was also studied (stepwise autoregulation). 3. Under control conditions (n = 12 dogs), the gain of the transfer function started to decrease, indicating improving autoregulation, below 0.06-0.15 Hz (t = 7-17 s). At 0.027 Hz a prominent peak of high gain was found. Below 0.01 Hz (t > 100 s), the gain reached a minimum (maximal autoregulation) of -6.3 +/- 0.6 dB. The stepwise autoregulation (n = 4) was much stronger (-19.5 dB). The time delay of the transfer function was remarkably constant from 0.03 to 0.08 Hz (high frequency (HF) range) at 1.7s and from 0.0034 to 0.01 Hz (low frequency) (LF) range) at 14.3 s, respectively. 4. Nifedipine, infused into the renal artery, abolished the stepwise autoregulation (-2.0 +/- 1.1 dB, n = 3). The gain of the transfer function (n = 4) remained high down to 0.0034 Hz; in the LF range it was higher than in the control (0.3 +/- 1.0 dB, P < 0.05). The time delay in the HF range was reduced to 0.5 s (P < 0.05). 5. After ganglionic blockade (n = 7) no major changes in the transfer function were observed. 6. Under furosemide (frusemide) (40 mg + 10 MG h-1 or 300 mg + 300 mg h-1 i.v..) the stepwise autoregulation was impaired to -7.8 +/- 0.3 or 6.7 +/- 1.9 dB, respectively (n = 4). In the transfer function (n = 7 or n = 4) the peak at 0.027 Hz was abolished. The delay in the LF range was reduced to -1.1 or -1.6 s, respectively. The transfer gain in the LF range (-5.5 +/- 1.2 or -3.8 +/- 0.8 dB, respectively) did not differ from the control but was smaller than that under nifedipine (P < 0.05). 7. It is concluded that the ample capacity for regulation of RBF is only partially employed under physiological conditions. The abolition by nifedipine and the negligible effect of ganglionic blockade show that above 0.0034 Hz it is almost exclusively due to autoregulation by the kidney itself. TGF contributes to the maximum autoregulatory capacity, but it is not required for the level of autoregulation expended under physiological conditions. Around 0.027 Hz, TGF even reduces the degree of autoregulation.