THE MECHANISM OF ACTION OF MUREXINE ON NEUROMUSCULAR TRANSMISSION IN THE FROG

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Abstract
Murexine (urocanoylcholine, [2-β-imidazol-4(5)-ylacryloyloxyethyl]trimethylammonium chloride hydrochloride) produced a contracture like acetylcholine in the frog rectus and a neuromuscular block in the rat diaphragm which was not relieved by neostigmine but was antagonized by hexamethonium. Using the foot muscle of the frog, electrical recordings showed that murexine produced a neuromuscular block and depolarized the end-plate region. These effects were similar to those seen with suxamethonium, decamethonium and acetylcholine. While murexine had the same depolarizing potency as decamethonium, it was only one-tenth as active as suxamethonium and acetylcholine. It was concluded that murexine could be classified as a “depolarizing type” of neuromuscular blocking agent but was less potent than suxamethonium.