AJP - Regulatory, Integrative and Comparative Physiology, Vol 236, Issue 5 302-R306, Copyright © 1979 by American Physiological Society
Effect of brain 5-hydroxytryptamine alterations on reflex bradycardia in rats
M. T. Lin and S. I. Chern
The vasopressor and bradycardia responses to an intravenous 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. However, brain serotonin alteration did
produce some influences on 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 produced a significant reduction in reflex bradycardia compared
to the controls. In contrast, depleting 5-HT contents in brain with either
p-chlorophenylalanine (PCPA) or 5,7-dihydroxytryptamine (5,7-DHT) led to an
enhancement of epinephrine-induced bradycardia. Moreover, the enhanced
reflex bradycardia induced by PCPA treatment was readily blocked by the
replacement of the depleted brain 5-HT with 5-HTP and Ro 4-4602. The
results suggest that 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.
