Modulating effect of central adrenergic neurones on a vagally mediated cardioinhibitory reflex

Pentobarbital-anaesthetized dogs were pretreated with the β-adrenoceptor blocking agent, KÖ 592, 5 mg/kg, and blood pressure and heart rate were measured continuously. Angiotensin (ANG), 0.0125–0.3 μg/kg, i.v., produced a rise in blood pressure accompanied by a reflex fall in heart rate. The α-adrenoceptor inhibiting drugs phentolamine, 5 mg/kg, i.v., or 0.5 mg/kg, intracisternally (i.ci.), and chlorpromazine, 0.5–1 mg/kg, i.ci., significantly suppressed the reflex bradycardia of ANG, whereas 0.5 mg/kg phentolamine i.v. was ineffective. In dogs pretreated with reserpine, 2.0 mg/kg, s.c., 18 hr, and KÖ 592 (as above) ANG regularly produced a reflex bradycardia which was not influenced by phentolamine, 0.5 mg/kg, i.ci.; the reflex bradycardia was potentiated by clonidine, 1 μg/kg, i.ci., and subsequent i.ci. injection of phentolamine reduced the reflex to the pre-clonidine value. Following pretreatment with atropine at a dose of 1.0 mg/kg, the reflex bradycardia of ANG was not changed by 0.5 mg/kg phentolamine i.ci. The conclusion is drawn, that cardio-inhibiting reflexes effected by the vagus are facilitated by adrenergic neurones within the central nervous system.