Central depression of carotid baroreceptor pressor response, arterial pressure and heart rate by 5-hydroxytryptophan: influence of supracollicular areas of the brain.

5-Hydroxytryptophan (5-htp) administered into the fourth cerebral ventricle of cats decreased resting arterial blood pressure, preganglionic sympathetic nerve activity and heart rate in both intact brain and midcollicular decerebrate preparations. The increases in sympathetic nerve discharge and blood pressure in response to bilateral carotid occlusion were reduced after 5-HTP administration when the brain was intact but not in midcollicular decerebrate preparations. Resting arterial pressure, heart rate and bilateral carotid occlusion response were not affected when the distribution of 5-HTP was confined to neural structures rostral to the midcollicular level by injection into the third or lateral cerebral ventricle with the cerebral aqueduct cannulated for drainage. Prior intracerebroventricular administration of an L-amino acid decarboxylase inhibitor (Ro 4-4602) prevented the effects of 5-HTP, indicating that depression is mediated via conversion to serotonin. These results suggest that serotenergic stimulation in the caudal brainstem or spinal cord produces depression of sympathetic outflow and decreases arterial blood pressure and heart rate. The bilateral carotid occlusion response is depressed by the brainstem serotonergic mechanisms which require the integrity of neural pathways connecting sub- and supracollicular areas of the brain. The possibility of reciprocal influence by the central serotonergic and adrenergic systems in cardiovascular control is discussed.