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ACTIONS OF MECAMYLAMINE, DIMECAMINE, PEMPIDINE AND THEIR TWO QUATERNARY METHO‐SALTS AT THE NEUROMUSCULAR JUNCTION
Author(s) -
BLACKMAN J. G.,
RAY C.
Publication year - 1964
Publication title -
british journal of pharmacology and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0366-0826
DOI - 10.1111/j.1476-5381.1964.tb01543.x
Subject(s) - mecamylamine , neostigmine , postsynaptic potential , chemistry , neuromuscular junction , decamethonium , methiodide , acetylcholine , curare , neuromuscular blocking agents , stimulation , pharmacology , neuroscience , acetylcholine receptor , anesthesia , biology , biochemistry , medicine , receptor
Mecamylamine, dimecamine and pempidine differed in neuromuscular‐blocking activity on the isolated phrenic nerve‐diaphragm preparation of the rat from the corresponding methiodides by a factor of less than two. It was concluded that the active component of each amine was the cation acting extracellularly. The finding that the neuromuscular‐blocking activity of mecamylamine at p H 6.7 was similar to the activity at p H 7.7 did not refute this conclusion. Mecamylamine, dimecamine methiodide, dimecamine and pempidine, at concentrations insufficient to cause block, could increase the twitch response of the rat diaphragm; the ability to do this increased in the above order. With pempidine (the most active compound) this effect, on the isolated sartorius muscle of the frog, was a direct action. During steady partial block by each of the compounds, the responses to brief tetanic stimulation, to neostigmine and to an increase in calcium concentration were similar to those observed during block by tubocurarine. From indirect evidence, pempidine methiodide appeared both to enhance the release of acetylcholine from motor‐nerve terminals and to cause postsynaptic block.