The goal of this study was to determine the degree of sympathetic postganglionic neuronal loss required to impair cardiovascular-related sympathetic activity. To produce neuronal loss separate groups of rats were treated daily with guanethidine for either 5days or 11days, followed by a recovery period. Sympathetic activity was measured by renal sympathetic nerve activity (RSNA). Stereology of thoracic (T13) ganglia was performed to determine neuronal loss. Despite loss of more than two thirds of neurons in T13 ganglia in both treated groups no effect on resting blood pressure (BP) or heart rate (HR) was detected. Basal RSNA in rats treated for 5days (0.61±0.10μV∗s) and 11days (0.37±0.08μV∗s) was significantly less than vehicle-treated rats (0.99±0.13μV∗s, p<0.05). Increases in RSNA by baroreceptor unloading were significantly lower in 5-day (1.09±0.19μV∗s) and 11-day treated rats (0.59±0.11μV∗s) compared with vehicle-treated rats (1.82±0.19μV∗s, p<0.05). Increases in RSNA to chemoreceptor stimulation were significantly lower in 5-day treated rats (1.54±0.25μV∗s) compared with vehicle-treated rats (2.69±0.23μV∗s, p<0.05). Increases in RSNA in 11-day treated rats were significantly lower (0.75±0.15μV∗s, p<0.05) compared with both vehicle-treated and 5-day treated rats. A positive correlation of neurons to sympathetic responsiveness but not basal activity was detected. These data suggest that diminished capacity for reflex sympathetic responsiveness rather than basal activity alone must be assessed for complete detection of neurophysiological cardiovascular impairment.
Keywords: Baroreceptor; Chemoreflex; Guanethidine; Sympathetic postganglionic neuron.
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