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1 Department of Pharmacology, Schools of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
A comparison was made of the effects on transmission in a sympathetic ganglion of calcium chloride and atropine. Unlike atropine, calcium chloride evoked ganglionic depolarization which was blocked by hexamethonium. Calcium chloride (0.25 to 5.0 mg) enhanced the ganglionic depolarization produced by ACh. The postganglionic firing by ACh was unchanged or enhanced by small doses of calcium chloride (0.25 to 1 mg) and depressed by larger doses (2 to 5 mg). These actions of the calcium ions can be attributed either to a presynaptic action which resulted in the release of ACh or to an influx of calcium ions into the ganglion cells. Furthermore, the depression by calcium of postganglionic firing produced by ACh at a time when the ganglionic depolarization evoked by ACh was enhanced is probably a reflection of the depolarizing and stabilizing properties of the ion.
Similarities between the actions of calcium chloride and atropine include (1) preferential blockade of the second component in the ganglionic response to injected ACh, (2) blockade of the postganglionic firing produced by methacholine (MCh), and (3) the antagonism of the ganglionic blockade produced by ACh, MCh, and tetramethylammonium. These findings indicate that ganglionic atropine-sensitive sites are extremely sensitive to blockade by nonspecific neuronal stabilizing agents.
Accepted on April 27, 1964