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). 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). 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 1.7 s and from 0.0034 to 0.01 Hz (low frequency (LF) range) at 14.3 s, respectively. 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). After ganglionic blockade (n= 7) no major changes in the transfer function were observed. 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). 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.

The aim of this study was to investigate the influence of the mean level and phasic modulation of NO on the dynamic autoregulation of renal blood flow (RBF). Transfer functions were calculated from spontaneous fluctuations of RBF and arterial pressure (AP) in conscious resting dogs for 2 h under control conditions, after NO synthase (NOS) inhibition [ N G-nitro-l-arginine methyl ester hydrochloride (l-NAME)] and afterl-NAME followed by a continuous infusion of an NO donor [ S-nitroso- N-acetyl-dl-penicillamine (SNAP)]. After l-NAME ( n = 7) AP was elevated, heart rate (HR) and RBF were reduced. The gain of the transfer function above 0.08 Hz was increased, compatible with enhanced resonance of the myogenic response. A peak of high gain around 0.03 Hz, reflecting oscillations of the tubuloglomerular feedback (TGF), was not affected. The gain below 0.01 Hz, was elevated, but still less than 0 dB, indicating diminished but not abolished autoregulation. Afterl-NAME and SNAP ( n = 5), mean AP and RBF were not changed, but HR was slightly elevated. The gain above 0.08 Hz and the peak of high gain at 0.03 Hz were not affected. The gain below 0.01 Hz was elevated, but smaller than 0 dB. It is concluded that NO may help to prevent resonance of the myogenic response depending on the mean level of NO. The feedback oscillations of the TGF are not affected by NO. NO contributes to the autoregulation below 0.01 Hz due to phasic modulation independent of its mean level.

This study tests whether the power spectrum of blood pressure (BP) provides information toward the sympathovagal balance of BP control by comparing the BP (femoral arterial catheter) spectrum with the spectrum of the efferent sympathetic nerve activity (SNA, bipolar electrode around splanchnic nerve). A remarkable resemblance between both spectra was found. A high-frequency component (HF) linked to respiration and a slower fluctuation type between 0.15 and 0.6 Hz (LF) were identified. There was a large and significant coherence only in the HF range of the BP and SNA power spectrum (P < 0.01). The phase lag of SNA and BP was roughly 200 ms. The recordings were repeated during pharmacological blockade in nine Wistar-Kyoto rats (WKY) and nine spontaneously hypertensive rats (SHR). alpha 1-Adrenoceptor blockade (prazosin) reduced the proportional LF power of BP in both rat strains (WKY P < 0.01, SHR P < 0.05) in favor of HF (WKY P < 0.01, SHR P < 0.01). Parasympathetic blockade (methylscopolamine) had no effect on proportions of power. Similarly, there were no significant differences in the proportional HF and LF power spectra of WKY and SHR. These data provide direct evidence for a relationship between the BP and SNA power spectra; however, only the acute changes in the sympathetic tone changed the LF-HF relationship.

Although angiotensin II (ANGII) exerts an important influence on the mean level of renal blood flow (RBF) and contributes to the fine tuning of glomerular filtration rate, the contribution of ANGII to the autoregulation of RBF is believed currently to be negligible (Navar et al. 1996). This view has been derived from studies in which the autoregulation of RBF had been assessed by the classical method of stepwise artificial reductions in renal artery pressure (RAP) (Abe et al. 1976; Arendshorst & Finn, 1977; Hall et al. 1977; Persson et al. 1988).However, under physiological conditions, fluctuations in RAP occur more dynamically and the process of RBF autoregulation itself exhibits a characteristic dynamic response pattern (Daniels et al. 1990; Holstein-Rathlou et al. 1991; Cupples et al. 1996; Just et al. 1998b). Therefore, several possibilities for a contribution from the renin-angiotensin system remain, which might have escaped detection when using the classical stepwise method. There are at least three possible ways in which ANGII could play a role in short-term autoregulation of RBF. First, ANGII might be involved (either directly or by modulating other mechanisms) in a frequency range that is faster than the 2-5 min duration of the artificial pressure steps, similar to the effects of nitric oxide (Just et al. 1999). Second, the total autoregulatory capacity is used only partially under physiological conditions (Just et al. 1998b), and this limited level of regulation might well be modified by ANGII. Finally, even if the ANGII does not actively participate in basal autoregulation, it might alter the relative contribution of those mechanisms that are involved.At present, RBF autoregulation is thought to be brought about by the myogenic response and tubuloglomerular feedback (TGF) (Navar et al. 1996) and perhaps by an additional slower mechanism (Just et al. 2001)