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1 Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, 05508-900 Sao Paulo, Brazil; and 2 Department of Pharmacology and Toxicology, Wright State University School of Medicine, Dayton, Ohio 45401
Previous work demonstrated that
oxytocinergic projections to the solitary vagal complex are involved in
the restraint of exercise-induced tachycardia (2). In the
present study, we tested the idea that oxytocin (OT) terminals in the
solitary vagal complex [nucleus of the solitary tract (NTS)/dorsal
motor nucleus of the vagus (DMV)] are involved in baroreceptor reflex
control of heart rate (HR). Studies were conducted in male rats
instrumented for chronic cardiovascular monitoring with a cannula in
the NTS/DMV for brain injections. Basal mean arterial pressure and HR
and reflex HR responses during loading and unloading of the
baroreceptors (phenylephrine/sodium nitroprusside intravenously) were
recorded after administration of a selective OT antagonist
(OTant) or OT into the NTS/DMV. The NTS/DMV was selected
for study because this region contains such a specific and dense
concentration of OT-immunoreactive terminals. Vehicle injections served
as a control. OT and OTant changed baroreflex control of HR
in opposite directions. OT (20 pmol) increased the maximal bradycardic
response (from 
56 ± 9 to 75 ± 11 beats/min), whereas
receptor blockade decreased the bradycardia (from 61 ± 13 to
35 ± 2 beats/min). OTant also reduced the operating
range of the reflex, thus decreasing baroreflex gain (from 5.68 ± 1.62 to 2.83 ± 1.05 beats · min
1 · mmHg1). OT
injected into the NTS/DMV of atenolol-treated rats still potentiated
the bradycardic responses to pressor challenges, whereas OT injections
had no effect in atropine-treated rats. The brain stem effect was
specific because neither vehicle administration nor injection of OT or
OTant into the fourth cerebral ventricle had any effect.
Our data suggest that OT terminals in the solitary vagal complex
modulate reflex control of the heart, acting to facilitate vagal
outflow and the slowdown of the heart.
immunohistochemistry; oxytocin receptors; nucleus of the solitary tract; dorsal motor nucleus of the vagus; fourth ventricle; blood pressure; reflex bradycardia; reflex tachycardia
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