Cholinergic inhibition of adrenergic transmission in the dog retractor penis muscle

Abstract

Muscarinic, cholinergic depression of adrenergic excitatory transmission was investigated by the microelectrode method in isolated dog retractor penis muscle. Electrical stimulation of the intramural nerves with single or repetitive stimuli elicited adrenergic contractions and excitatory junction potentials (e.j.p.s). The mechanical response and e.j.p. were suppressed by physostigmine (5 x 10(-7) g/ml) and carbachol (up to 5 x 10(-8) g/ml) without changing the sensitivity of the muscle to noradrenaline and muscle membrane resistance measured by electrotonic potentials. Atropine reversed the drug-induced attenuation of these responses, but atropine itself had no effect on them. Carbachol at 5 x 10(-8) g/ml, where the e.j.p. was blocked, caused a depolarization of the muscle membrane (less than 5 mV), whereas the same extent of depolarization produced by high K solution resulted in only a small decrease in e.j.p. amplitude. These results suggest that excitatory adrenergic transmission in the dog retractor penis muscle is depressed prejunctionally by a cholinergic mechanism.