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Failure of the calcium channel activator, Bay K 8644, to increase the release of acetylcholine from nerve terminals in brain and diaphragm
Author(s) -
Doležal Vladimír,
Tuček Stanislav
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb11239.x
Subject(s) - acetylcholine , depolarization , calcium , chemistry , biophysics , free nerve ending , activator (genetics) , endocrinology , medicine , anatomy , biology , biochemistry , receptor , organic chemistry
1 The calcium channel activator Bay K 8644 did not increase the release of acetylcholine from rat brain cortex prisms incubated in the presence of 3 mmol l −1 or 25 mmol l −1 K + nor from rat diaphragms incubated in the presence of 5 mmol l −1 or 25 mmol l −1 K + . It also did not influence the release of acetylcholine from cortex prisms incubated in the presence of 25 mmol l −1 K + and of lowered concentrations of Ca 2+ ions. 2 It is concluded that the voltage‐dependent Ca 2+ channels in the nerve terminals, responsible for the depolarization‐induced influx of Ca 2+ ions into the nerve terminals and thus for the depolarization‐evoked release of acetylcholine from the nerve terminals, are different from the voltage‐dependent Ca 2+ channels in the heart and smooth muscle cells.