Clonidine inhibits electrodermal potentials induced by preganglionic stimulation.

The electrodermal potential (EDP) recorded with surface electrodes between the palm and the shaven back of the right forepaw of anaesthetized and vagotomized cats was taken as a measure of the activity of cholinergic-sympathetic sudomotor nerves. EDPs were induced by preganglionic electrical stimulation of the stellate ganglion for 2 s with trains of DC pulses (2 ms duration, 0.5-128 Hz) at regular intervals of 60 s. The EDPs amounted to 12 mV and increased little with stimulation rate (14 mV). The i.v. injection of 30 micrograms/kg of the alpha 2-adrenergic agonist clonidine did not change the EDPs significantly. A consistent result was obtained in cats pretreated i.p. with 5 mg/kg reserpine 18 h beforehand for depletion of catecholamines. Three hours after the i.v. injection of 3 mg/kg guanethidine, clonidine (30 micrograms/kg i.v.) induced significant reduction of EDPs in the lower range of the stimulation rate but did not affect those at 16 and 32 Hz. Partial blockade of ganglionic nicotinic receptors by i.v. infusion of 0.08-0.3 mg/kg per min hexamethonium diminished EDPs (1 Hz) by 30-50%. Under these conditions the i.v. injection (30 micrograms/kg) or topical application of 1 microgram clonidine to the right stellate ganglion inhibited EDPs at all rates of stimulation. The inhibitory effects of clonidine could be antagonized by 200 micrograms/kg yohimbine i.v. Partial ganglionic blockade by i.v. infusion of the depolarizing blocker suxamethonium (0.2-0.4 mg/kg per min) decreased EDPs. However, the topical application of 1 microgram clonidine to the stellate ganglion during infusion of suxamethonium caused no further decrease.(ABSTRACT TRUNCATED AT 250 WORDS)