Sympathetic inhibition and vasopressin mediation during centrally induced responses to serotonin in rats.

To study mechanisms underlying the cardiovascular effects of centrally administered serotonin, we recorded responses to intracerebroventricular (i.c.v.) injections of serotonin in urethane-anesthetized rats. Dose-related increases in blood pressure accompanied by reductions in heart rate and sympathetic nerve firing were elicited consistently. The diminution in sympathetic nerve activity implies that while sympathetic inhibition could contribute to the bradycardia, sympathetic activation alone cannot account for the pressor response. Pressor and bradycardic responses must have been caused by activation of specific serotonergic receptors in the brain because both responses were inhibited following serotonin blockade produced by i.c.v. injection of methysergide. By contrast, intravenous injection of a vasopressin antagonist inhibited the pressor response selectively, thereby suggesting that peripheral mediation of the pressor (but not the bradycardic) response involves release of endogenous vasopressin. Collectively, our results are compatible with the interpretation that i.c.v.-injected serotonin acts on serotonergic brain receptors to elevate blood pressure by releasing endogenous vasopressin, and slow the heart through sympathetic inhibition.