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Effects of Ca2+ blockers on the various types of stimuli-induced acetylcholine release from guinea pig lleum myenteric plexus.
Author(s) -
Keiji Yokoyama,
Osamu Yagasaki
Publication year - 1990
Publication title -
the japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.52.109
Subject(s) - verapamil , acetylcholine , nicotine , chemistry , procaine , pharmacology , diltiazem , stimulation , channel blocker , extracellular , calcium , endocrinology , medicine , biochemistry , organic chemistry
In the present study, we investigated the effects of various Ca2+ blockers on the release of acetylcholine (ACh) induced by nicotine, electrical field stimulation (EFS) and high-K+. Cd2+ markedly depressed the ACh release due to these stimuli. Verapamil inhibited the nicotine-induced ACh release remarkably and the EFS- or the high-K(+)-induced ACh release to a lesser extent. Since the nicotine- and the EFS-induced ACh releases were inhibited by procaine, the local anesthetic property of verapamil likely contributes in part to the inhibition. Diltiazem abolished the nicotine-induced ACh release completely but did not affect the EFS-induced release and significantly increased the high-K(+)-induced ACh release. These results suggest the absolute requirement for extracellular Ca2+ in the release of ACh induced by nicotine as well as EFS and high-K+. In addition, these stimuli may open the same Ca2+ channel to evoke ACh release.

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