Abstract:
Blood pressure displays an oscillation at 0.1 Hz in humans established to be due to sympathetic nerve activity (SNA). However, the mechanisms that control the strength and frequency of this oscillation are poorly understood. The kidney is richly innervated and thus understanding how SNA and renal function interact may be important in understanding the origin of oscillations in, and the general control of blood pressure. In pentobaritone anaesthetised rabbits, the left renal nerves were exposed and electrically stimulated and the corresponding changes in renal haemodynamics recorded. Initially, regional differences in the vascular responses to renal nerve stimulation were assessed by monitoring the responses of laser Doppler flux to steady-state renal nerve stimulation at different depths below the cortical surface. Subsequently how renal blood flow responded to different frequencies of electrical stimulation was assessed by applying pseudo-random binary sequence (PRBS) based electrical stimulation to the renal nerves. The PRBS stimulation delivers all frequencies 0-1 Hz with equal spectral power, which allowed a transfer function model to be calculated for the frequency response. In attempting to identify the mediators of this frequency response further experiments were undertaken in which either a range of vasoactive agents were administered or renal perfusion pressure was altered, independent of systemic pressure, using an extracorporeal circuit. In conclusion, we have found that the frequency response of the renal vasculature to renal nerve stimulation is a complex response comprising of a low-pass filter with regions of constant gain and is well described by a 2-zero/4-pole transfer function with a pure time delay. This dynamic response of the renal vasculature was not altered by either infusion of vasoactive agents that changed renal blood flow by ± 30 % or by different levels of renal perfusion pressure, despite these interventions affecting the response to steady-state nerve stimulation. Together, these results suggest that the steady-state and dynamic neural control of the renal vasculature are relatively independent.