Efferent mechanisms mediating renal sodium and water excretion induced by centrally administered serotonin.

Treatments that increase central extracellular serotonin (5-HT) also increase Na excretion. Efferent renal sympathetic nerve activity (ERSNA) contributes to the control of Na and water reabsorption. To determine whether renal nerves play a role in the 5-HT-induced natriuresis, we examined the effect of intracerebroventricular (icv) injection of vehicle or 5-HT (20 micrograms) on Na, K, and urine excretion rates, as well as mean arterial pressure and heart rate in unanesthetized, hydrated rats with renal nerves intact or sectioned. Renal denervation attenuated the natriuresis produced by 5-HT but not the antidiuresis observed 15-30 min after injection. Central 5-HT produced brief pressor and bradycardic responses, followed by continued bradycardia and hypotension, which were more pronounced in intact rats. In other experiments, circulating levels of arginine vasopressin (AVP) and plasma atrial natriuretic polypeptide (ANP) were measured 15 min after icv injection of 5-HT. 5-HT significantly increased circulating AVP, but plasma ANP remained unchanged. These results suggest that renal nerves participate in the natriuresis elicited by centrally administered 5-HT through a decrease in ERSNA. The antidiuresis observed after central 5-HT may be due to an increase in AVP release.