THE EFFECTS OF BARIUM AND OTHER INORGANIC CATIONS ON SYMPATHETIC GANGLIA

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

Depolarization and postganglionic firing of the superior cervical ganglion of cats occurred following the intraarterial administration of barium chloride. These ganglionic responses to barium were depressed by hexamethonium or mecamylamine. The mean threshold dose of barium required to evoke these responses in denervated ganglia was greater than in normal ganglia. Three possibe mechanisms for the barium-induced responses were considered. First, the possibility was discussed that barium acted by causing the release of ACh from preganglionic nerve endings. Second, it was suggested that the responses to barium resulted from a penetration by the divalent cation of ganglionic cellular membranes. Third, a possible interference by barium of the permeability to potassium ions was considered as a basis for the depolarization produced by barium.

Treatment of the ganglia with barium unmasked an atropine-sensitive component in the postganglionic response to ACh and enhanced the postganglionic firing produced by MCh. These actions were in contrast to the previously reported findings with calcium ions. Like calcium, barium also antagonized the blockade of transmission produced by tetramethylammonium. In addition, barium antagonized the ganglionic actions of veratridine. The effects of veratnidine on sympathetic ganglia included an enhancement of the ganglionic depolarization evoked by ACh or MCh, a reduction of the ganglionic hyperpolarization evoked by MCh, and an enhancement of the postganglionic firing produced by ACh or MCh.