Methylpentynol, paraldehyde, amylobarbitone and procainamide blocked transmission through the cat superior cervical ganglion, and antagonized the ganglion-stimulating actions of acetylcholine and carbachol injected intra-arterially to the ganglion. Comparison with the effects of tetraethylammonium indicated that the impaired response to acetylcholine could not wholly account for the failure of transmission, which suggested that an impaired release of transmitter substance was a contributory factor. Methylpentynol, paraldehyde and procainamide also blocked the ganglion-stimulating action of potassium chloride. In contrast, amylobarbitone and pentobarbitone did not block the stimulating action of potassium chloride, but antagonized specifically the actions of acetylcholine and carbachol. The anti-acetylcholine activities of the two barbiturate drugs at this site accord with their relative ganglion-blocking activities. It is concluded that the ganglion-blocking action of methylpentynol, paraldehyde and procainamide arises from a nonspecific depression of both presynaptic and postsynaptic elements in the ganglion, but that barbiturate compounds act more specifically on the acetylcholine receptor.
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Brown et al. (1964) studied this question.
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