Abstract
The action of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343) was studied on the superior cervical ganglion and inferior mesenteric ganglion in cats, and compared to that of DMPP and pilocarpine. Effects were measured by contraction of the nictitating membrane or by post-ganglionic action potentials, respectively.
McN-A-343 caused contraction of the nictitating membrane in both normal and decentralized preparations; it had no direct action on the post-ganglionic effector organ. Its ganglionic stimulant action was blocked by tetramethylammonium, cocaine, morphine, and especially by atropine, but not by tetraethylammonium, hexamethonium or nicotine. It greatly potentiated the effects of potassium chloride on the nictitating membrane and on the blood pressure. It potentiated the responses to submaximal electrical preganglionic stimulation.
McN-A-343 initially antagonized the contracting effect of acetyleholine on the nictitating membrane, but later potentiated the response to acetylcholine.
Preganglionic stimulation, after nicotine, relaxed the contraction of the nictitating membrane obtained with McN-A-343. This relaxation was not affected by Dibenamine. ACh injected to the ganglion similarly relaxed the nictitating membrane contracted by either McN-A-343 or by sustained preganglionic stimulation.
McN-A-343 caused a marked increase in the discharges of the inferior mesenteric ganglion; its action was blocked by atropine but not by hexamethomum.
McN-A-343 caused a contracture of the isolated frog rectus muscle and decreased its response to ACh.
The action of McN-A-343 on sympathetic ganglia corresponds to that of a non-nicotinic ganglion stimulant. Its spectrum of action resembles in many, but not all aspects, that of pilocarpine. Its site of action on the ganglion cell appears to be the same as that of atropine, possibly the LN receptor postulated by Eccles and Libet (1961).
Footnotes
- Accepted January 28, 1963.
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