Effect of brain 5-hydroxytryptamine alterations on reflex bradycardia in rats

Abstract
The vasopressor and bradycardia responses to an i.v. dose of epinephrine were assessed in saline-controlled, 5-hydroxytryptamine-(5-HT) depleted and 5-HT-potentiated rats. Regardless of the previous treatment epinephrine produced an insignificant change in the basal levels of mean arterial pressure and heart rate. Brain serotonin changes did influence the reflex bradycardia in response to an elevation in arterial pressure. Elevating 5-HT contents in brain with 5-hydroxytryptophan (5-HTP) after peripheral decarboxylase inhibition with Ro 4-4602 [benserazide] produced a significant reduction in reflex bradycardia compared to the controls, but depleting 5-HT contents in brain with eiter p-chlorophenylalanine (PCPA) or 5,7-dihydroxytryptamine (5,7-DHT) enhanced epinephrine-induced bradycardia. The enhanced reflex bradycardia induced by PCPA treatment was blocked by the replacement of the depleted brain 5-HT with 5-HTP and Ro 4-4602. Apparently the serotoninergic systems play a role in the elaboration or modulation of reflex bradycardia. Specifically, 5-HT appears to inhibit reflex bradycardia since its depletion facilitated and its elevation inhibited reflex bradycardia.

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