Baroreflex control of heart rate by oxytocin in the solitary-vagal complex.

Abstract

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 (OT(ant)) 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 OT(ant) 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). OT(ant) also reduced the operating range of the reflex, thus decreasing baroreflex gain (from -5.68 +/- 1.62 to -2.83 +/- 1.05 beats x min(-1) x mmHg(-1)). 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 OT(ant) 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.