Degeneration of capsaicin-sensitive sensory nerves leads to increased salt sensitivity through enhancement of sympathoexcitatory response.

We have previously shown that 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. To test the hypothesis that the enhanced sympathoexcitatory response to a high salt intake contributes to the development of hypertension in this model, newborn Wistar rats were given 50 mg/kg capsaicin and/or 80 mg/kg guanethidine subcutaneously. Control rats were treated with vehicle. After the weaning period, male rats were grouped as the following and given a high sodium diet (4%) for 2 weeks: capsaicin and guanethidine coadministration (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 excretions were significantly lower in CAP than in CAP-GUA, GUA, and CON rats (P<0.05). Mean arterial pressure (mm Hg) 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 counterbalance the prohypertensive effect of the sympathetic nerves to maintain blood pressure within normal range during salt loading.