Е. В. Лукошкова

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml.min(-1).kg-1 for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 +/- 1 vs. 31 +/- 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of oscillations in each variable. Before hemorrhage, a rhythm at approximately 0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (< 0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies > 0.25 Hz was significantly less in intact than denervated rabbits (0.83 +/- 0.12 vs. 1.19 +/- 0.10 ml.min(-1).mmHg-1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These wer accompanied by increases in the spectral power of RBF at the same frequency. Arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

One of the new methods to evaluate the sensitivity of the baroreceptor-heart rate (HR) reflex involves the use of power spectral analysis to calculate the transfer function between blood pressure and HR. We assess the applicability and reproducibility of the baroreflex gain estimated by this method with traditional invasive techniques that induce ramp changes in mean arterial pressure (MAP) in conscious rabbits. Renal sympathetic nerve activity recordings are used to identify the mid-frequency band, and we also identify coherent fluctuations of MAP and HR with a 1.8 s phase delay, consistent with a baroreflex relationship and therefore appropriate to estimate the cross spectral transfer function.

While several papers support the physiological and clinical relevance of indices quantifying the sensitivity of spontaneous baroreflex control of heart rate (BRS), 1 Lipman et al 2 claim that they are unable to properly explore baroreflex function because spontaneous BRS was found to be quantitatively different from BRS values provided by the vasoactive drug injection technique and is unrelated to common carotid artery distensibility. We believe that this conclusion is not supported by Lipman's data, for the following reasons.