Cns actions of serotonin on cardiovascular function: non
-adrenergic, non-cholinergic mechanisms.
Dedeolu, Alpaslan, and Laurel A. Fisher.
Department of Physiology, The Ohio State University College of
Medicine, Columbus, Ohio 43210
APStracts 3:0076R, 1996.
The present studies investigated the mechanisms mediating the
cardiovascular changes induced by intracerebroventricular (icv)
injection of serotonin (5-HT; 100 nmol) in conscious rats. At 5 min
after 5-HT injection, arterial pressure and plasma levels of
epinephrine were elevated and heart rate was reduced. The pressor
response was abolished by either bilateral adrenalectomy or by
pretreatment with chlorisondamine plus vasopressin V1 receptor
antagonist. The bradycardic response was attenuated by pretreatment
with chlorisondamine or a combination of methylatropine, propranolol
and vasopressin V1 receptor antagonist. At 20 min postinjection,
arterial pressure and heart rate were both decreased. The reduction
of heart rate at this time point was not blocked by the following
pretreatments given alone or in combination: methylatropine,
propranolol, vasopressin V1 and V2 receptor antagonists, adenosine A1
receptor antagonist, angiotensin converting enzyme inhibitor and
chlorisondamine. These results suggest that immediately after icv
injection of 5-HT, arterial pressure is elevated through the release
of epinephrine and vasopressin and that heart rate is reduced via
reciprocal changes in cardiac parasympathetic and sympathetic tone.
In contrast, adrenergic, cholinergic, vasopressinergic, purinergic
and angiotensinergic mechanisms do not mediate the bradycardia
observed at 20 min postinjection.
Received 3 August 1995; accepted in final form 26 February 1996.
APS Manuscript Number R490-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96