Neuronal Control of Salt Sensitivity: Role of Sensory and Sympathetic Nerves
Neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to a salt load with an increase in blood pressure and a decrease in natriuretic response (Wang, et al, Hypertension 1998;32:649-653). To test the hypothesis that the sympathetic nervous system contributes to the development of salt sensitive hypertension induced by sensory denervation, newborn Wistar rats were given 50mg/kg capsaicin and/or 80mg/kg guanethidine s.c.. Control rats were treated with vehicle. After the weaning period, male rats were grouped as the following and given high sodium diet (4%) for 2 weeks: capsaicin and guanethidine co-administration (CAP-GUA), capsaicin only (CAP), guanethidine only (GUA), and vehicle control (CON). Norepinephrine concentrations in the atrium were significantly lower in CAP-GUA and GUA than in CON rats (p<0.05). Twenty-four hour urine and sodium excretion was significantly lower in CAP than in CAP-GUA, GUA and CON rats (p<0.05). Mean arterial pressure (mmHg) was significantly higher in CAP (180±10) than in CAP-GUA (106±1), GUA (133±5), and CON (122±3) rats (p<0.05). Thus, sympathectomy restores the natriuretic response to a high salt intake and prevents the development of salt sensitive hypertension induced by sensory denervation. These data indicate that sensory nerves counterbalances the pro-hypertensive effect of the sympathetic nerves to maintain blood pressure within normal range during salt loading.