Clonidine inhibits nicotinic effects in ganglia of the cholinergic-sympathetic system

Abstract

The electrodermal potential (EDP) recorded with surface electrodes between the palm and the shaven back of the forepaws of anaesthetized cats was taken as a measure of sudomotor activity in response to submaximal activation of cholinergic-sympathetic efferents with the nicotinic ganglionic stimulant DMPP. The intravenous injection of 30 μg/kg clonidine inhibited EDPs in despinalized cats and in vagotomized cats with chronic denervation of the stellate ganglion. In vagotomized cats clonidine (30 μg/kg i.v.) shifted the dose-response curve of DMPP (4–256 μg/kg i.v.) to the right. An inhibitory effect was also observed in despinalized cats upon topical application of 0.1 and 1 μg clonidine to the stellate ganglion. In all preparations the inhibitory effect of clonidine could be antagonized by intravenous injection of 200 μg/kg yohimbine. As all substances used were also active when injected during arrest of blood flow to the foreleg by means of a tourniquet, actions at the level of the sweat gland could be excluded. The results lead to the conclusion that the activation of postsynaptic somadendritic α 2-adrenoceptors in sudomotor ganglia of the cholinergic-sympathetic nervous system inhibits the effects of nicotinic ganglionic stimulation. It is assumed that this action is due to the known ganglionic hyperpolarization induced by α 2-adrenoceptor stimulants.