Augmentation of vagal reflex bradycardia be central alpha2-adrenoceptors in the cat.

Vagal reflex bradycardia was induced in anaesthetized cats with high level spinal axotomy by electrical stimulation of either the carotid sinus nerves or a depressor nerve. In both preparations reflex bradycardia increased with the rate of stimulation. Injection of 1 microgram/kg clonidine into a lateral cerebral ventricle augmented reflex bradycardia in response to carotid sinus nerve stimulation while the same dose of clonidine was ineffective when given intravenously. The antagonistic effect of intracerebroventricular yohimbine (50 micrograms/kg) indicated that the effect of clonidine was due to its alpha2-agonistic action. In contrast to carotid nerve stimulation the reflex bradycardia in response to depressor nerve stimulation was affected neither by intracerebroventricular injection of clonidine (2 micrograms/kg) nor by yohimbine (100 micrograms/kg). It is concluded that in the cat, the function of the central parts of the baroreceptor reflex which originate from the carotid sinus area is augmented by stimulation of alpha2-adrenoceptors while the function of those parts originating from the aortic area is not.