AJP - Heart and Circulatory Physiology, Vol 272, Issue 2 894-H903, Copyright © 1997 by American Physiological Society
Hypothyroid-induced changes in autonomic control have a central serotonergic component
W. N. Henley and F. Vladic
Department of Biological Sciences and College of Osteopathic Medicine, Ohio University, Athens 45701, USA.
Three experiments were conducted in unanesthetized rats made hypothyroid
(Hypo) or maintained as euthyroid controls (Eu) to examine general
cardiovascular responsiveness [experiment I (Exp I)]; responsiveness to a
serotonin (5-HT2) agonist, dl-2,5-dimethoxy-4-iodoamphetamine [DOI
intracerebroventricularly; experiment II (Exp II)]; or responsiveness to a
5-HT(1A) agonist dl-8-hydroxydipropyl-aminotetralin hydrobromide [8-OH-DPAT
intracerebroventricularly; experiment III (Exp III)]. In Exp I, intravenous
infusions of phenylephrine and nitroprusside provided little evidence that
findings in Exp II and III were caused by generalized impairment in
cardiovascular responsiveness in Hypo. In Exp II and III, Eu and Hypo were
given either intra-arterial atropine or vehicle. Atropine significantly
elevated heart rate (Exp II and III) and mean arterial pressure (Exp II) in
Eu only. When compared with Eu, Hypo had a reduced pressor response (5.2
vs. 20.1%), an attenuated pulse pressure response (19.3 vs. 35.4%), and a
more robust bradycardia (-17.7 vs. -7.0%) in response to DOI. These
differences were atropine sensitive. In Exp III, Hypo had larger decrements
in mean arterial pressure (-9.0 vs. -5.1%), heart rate ( -13.9 vs. - 7.7%),
and body temperature (-4.5 vs. -2.7%) in response to 8-OH-DPAT in
comparison to Eu. Parasympathetic involvement in the differential responses
to 8-OH-DPAT was less clear than with DOI. Deranged autonomic control in
hypothyroidism may be caused, in part, by changes in central serotonergic
activity.
