The role of cardiac receptors in clonidine-induced vagal bradycardia.

In chloralosed, spinalized and beta-blocked cats, clonidine, 10 microgram/kg i.v. caused a vagally mediated bradycardia which was further analysed with particular attention to cardiopulmonary receptors. Cardiovascular deafferentiation, with preservation of vagal cardiac efferents, abolished the bradycardia. However, in animals with arterial baroreceptors denervated but with vagal cardiopulmonary pathways intact, clonidine decreased heart rate simultaneously with an increase in left atrial pressure to an extent known to activate cardiac receptors with unmyelinated vagal efferents. Clonidine somewhat enhanced the bradycardia to efferent vagal stimulation and also had a slight positive chronotropic effect on the non-innervated heart. The reflex bradycardia from electrical stimulation of unmyelinated cardiac afferents was augmented by the drug but not more than could be accounted for by the changed neuroeffector sensitivity. The data suggest that clonidine can reflexly augment vagal tone on the heart by an increased activity in vagal cardiac afferents, secondary to the drug's peripheral vasoconstrictor action, whereas no evidence for any central facilitation of these reflexes has been found.