Renal SNA as the primary mediator of slow oscillations in blood pressure during hemorrhage

Blood pressure contains a distinct low-frequency oscillation often termed t he Mayer wave. This oscillation is caused by the action of the sympathetic nervous system on the vasculature and results from time delays in the baror eflex feedback loop for the control of sympathetic nerve activity (SNA) in response to changes in blood pressure. In this study, we used bilateral ren al denervation to test the hypothesis that it is SNA to the kidney that con tributes a large portion of the vascular resistance associated with changes in the strength of the slow oscillation in blood pressure. In conscious ra bbits, SNA and blood pressure were measured during hemorrhage (blood withdr awal at 1.35 ml.min(-1).kg(-1) for 20 min). Spectral analysis identified a strong increase in power at 0.3 Hz in SNA and blood pressure in the initial compensatory phase of hemorrhage before blood pressure started to fall. Ho wever, in a separate group of renal denervated rabbits, although the power of the 0.3-Hz oscillation under control conditions in blood pressure was si milar, it was not altered during hemorrhage. Wavelet analysis revealed the development of low-frequency oscillations at 0.1 Hz in both intact and dene rvated animals. In conclusion, we propose that changes in the strength of t he oscillation at 0.3 Hz in arterial pressure during hemorrhage are primari ly mediated by sympathetic activity directed to the kidney.