INTERACTIONS BETWEEN THE CATECHOLAMINES AND GANGLIONIC STIMULATING AGENTS IN SYMPATHETIC GANGLIA

¹ Department of Pharmacology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

The relationship between the ganglionic potentials evoked by norepinephrine, (NE), epinephrinie (E) and isoproterenol (ISO) and the effects of these agents on the ganglionic stimulating actions of cholinergic and noncholinergic substances were studied in the superior cervical ganglion of the cat. The catecholamines, administered intraarterially in doses that produced marked effects on ganglionic transmission, did not alter the hexamethonium-sensitive postganglionic discharge evoked by acetylcholine (ACh) or nicotine. However, the former agents did unmask or enhance a late occurring atropinesensitive discharge to ACh. This action was potentiated by alpha adrenergic blocking agents and antagonized by beta adrenergic blocking agents. NE and E also exerted marked inhibitory and facilitatory actions on the atropine-sensitive postganglionic firing evoked by other agents (e.g., anticholinesterase agents, oxotremorine and acetyl--methylcholine). These actions were correlated with catecholamine-evoked ganglionic hyperpolarization and depolarization, respectively, and were blocked, respectively, by the alpha and beta blocking agents. ISO produced an enhancement of the atropine-sensitive firing and ganglionic depolarization. ISO also enhanced the postganglionic firing evoked by barium chloride, but depressed the firing produced by potassium chloride. The above findings provide additional support for the proposal that NE and E have both inhibitory and facilitatory actions on sympathetic ganglia and that these actions of the catecholamines are mediated by a hyperpolarization and depolarization of the ganglion cells, respectively. Furthermore, the blockade by ISO of the ganglionic response to potassium suggests that the catecholamine-evoked ganglionic depolarization may result from a reduction in the membrane permeability to potassium ions.

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