Renal hemodynamic responses to sustained suppression of central sympathetic outflow

Abstract

Chronic electrical stimulation of the carotid baroreflex causes sustained reductions in blood pressure by suppression of sympathetic activity (SA). The role of SA in controlling renal hemodynamic responses to chronic reductions in renal perfusion pressure is unknown. Therefore, we compared renal and systemic hemodynamics in normotensive dogs in which blood pressure was lowered consecutively for 2 weeks by either baroreflex activation (BA, low SA) or calcium channel blockade with amlodipine, 5mg/kg/day, (CCB, high SA). Both interventions caused a similar sustained reduction in mean arterial pressure (MAP) by ~18 mmHg. Glomerular filtration rate (GFR) responses were as follows: BA CCB Control 67.8±3.3 65.0±2.0 Week 1 59.3±2.4* 62.4±3.0 Week 2 59.7±2.3* 63.7±2.5 Recovery 64.3±2.5 64.2±2.2 P< 0.05 vs control GFR decreased by 10–15% during baroreflex activation while it was unchanged from control during CCB. Renal blood flow (RBF), measured continuously by ultrasound flow probes, decreased by 10–15% during baroreflex activation while its circadian pattern of variation was maintained. These data are consistent with the hypothesis that despite reduced MAP, sustained suppression of renal SA by BA chronically reduces Na+ reabsorption prior to the macula densa, initiating sustained preglomerular vasoconstriction, which results in lowering of GFR and RBF. As renal disease is commonly associated with hyperfiltration and glomerular hypertension, this effect may provide an additional benefit in hypertensive patients in which reductions in renal hyperfiltration are desirable.