Abstract
The hypothesis that nicotinic agonists other than acetylcholine act by releasing endogenous acetylcholine was examined using nerve-free cultures of chick embryonic skeletal muscle. All nicotinic agonists tested (acetylcholine, carbachol, DMPP, tetramethylammonium and nicotine) depolarized the cultured skeletal muscle fibres. The depolarization was antagonised by triethylcholine, hemicholinium-3, tetraethylammonium and hexamethonium, substances that have been suggested to act by preventing agonists acting on nerve terminals. The results confirm that triethylcholine, hemicholinium-3, tetraethylammonium and hexamethonium have postjunctional blocking actions. We conclude that nicotinic agonists act directly on cholinoreceptors and do not require the presence of endogenous acetylcholine.
Original language | English |
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Pages (from-to) | 131-134 |
Number of pages | 4 |
Journal | European Journal of Pharmacology |
Volume | 28 |
Issue number | 1 |
DOIs | |
Publication status | Published - 1 Jan 1974 |
Keywords
- acetylcholine receptors
- cultered skeletal muscle
- ganglion-blocking drugs
- hemicholinium-like drugs
- site of action
- 1,1 dimethyl 4 phenylpiperazinium
- 1,1 dimethyl 4 phenylpiperazinium iodide
- carbachol
- cholinergic receptor
- ganglion blocking agent
- hemicholinium 3
- hexamethonium
- tetramethylammonium
- drug antagonism
- in vitro study
- membrane depolarization
- muscle fiber culture