Renal hemodynamic effects of activation of specific renal sympathetic nerve fiber groups

To examine the effect of activation of a unique population of renal sympathetic nerve fibers on renal blood flow (RBF) dynamics, anesthetized rats were instrumented with a renal sympathetic nerve activity (RSNA) recording electrode and an electromagnetic flow probe on the ipsilateral renal artery. Peripheral thermal receptor stimulation (external heat) was used to activate a unique population of renal sympathetic nerve fibers and to increase total RSNA. Total RSNA was reflexly increased to the same degree with somatic receptor stimulation (tail compression). Arterial pressure and heart rate were increased by both stimuli. Total RSNA was increased to the same degree by both stimuli but external heat produced a greater renal vasoconstrictor response than tail compression. Whereas both stimuli increased spectral density power of RSNA at both cardiac and respiratory frequencies, modulation of RBF variability by fluctuations of RSNA was small at these frequencies, with values for the normalized transfer gain being ∼0.1 at >0.5 Hz. During tail compression coherent oscillations of RSNA and RBF were found at 0.3–0.4 Hz with normalized transfer gain of 0.33 ± 0.02. During external heat coherent oscillations of RSNA and RBF were found at both 0.2 and 0.3–0.4 Hz with normalized transfer gains of 0.63 ± 0.05 at 0.2 Hz and 0.53 ± 0.04 to 0.36 ± 0.02 at 0.3–0.4 Hz. Renal denervation eliminated the oscillations in RBF at both 0.2 and 0.3–0.4 Hz. These findings indicate that despite similar increases in total RSNA, external heat results in a greater renal vasoconstrictor response than tail compression due to the activation of a unique population of renal sympathetic nerve fibers with different frequency-response characteristics of the renal vasculature.