Effects of central serotonin on autonomic control of heart rate in intact and baroreceptor deficient rats

Abstract

The intracerebroventricular (i.c.v.) injection of serotonin (5-HT) increases blood pressure and decreases heart rate (HR) in conscious rats by activation of 5-HT 2/1C receptors. Since the bradycarbia is eliminated by pretreatment with a ganglionic or V 1-vasopressin antagonist, we proposed that the decrease in HR results from an effect on cardiac autonomic activity which is potentiated by vasopressin. The present study aimed first, to further characterize mechanisms by which the i.c.v. injection of 5-HT (2.5 μg) decreases HR in consious rats, and second to determine the cardiovascular responses to 5-HT (2.5 μg, i.c.v.) in rats with chronic sinoaortic deafferentation (SAD). In intact rats, the bradycardia elicited by 5-HT was eliminated by a combination of the muscarinic antagonist atropine and the β-adrenoceptor antagonist sotatol; neither antagonist was effective alone. In rats with SAD, 5-HT produced a larger increase in blood pressure and a marked tachycardia, both of which were eliminated by the 5-HT 2/1C antagonist LY 53857. Furthermore, in rats with SAD the 5-HT-induced increase in HR was blocked by sotalol alone. In conclusion, 5-HT (2.5 μg, i.c.v.) acts on cenrtal 5-HT 2/1C receptors to increase arterial pressure. In intact rats this decreases HR by vasopressin-potentiated activation of baroreceptor reflexes and subsequent increase in vagal tone and decrease in cardiac sympathetic tone. In the absence of baroreflexes, a direct central effect of 5-HT to produce a β-adrenoceptor-mediated cardioacceleration is unmasked.