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Dissociation between exocytosis and Ca 2+ ‐channel activity in mouse pancreatic β‐cells stimulated with calmidazolium (compound R24571)
Author(s) -
Kindmark Henrik,
Köhler Martin,
Larsson Olof,
Khan Akhtar,
Berggren Per-Olof
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00774-4
Subject(s) - exocytosis , dissociation (chemistry) , chemistry , microbiology and biotechnology , biophysics , stereochemistry , biochemistry , biology , secretion , organic chemistry
Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca 2+ through voltage‐gated Ca 2+ channels in mouse pancreatic β‐cells. Despite this fact, calmidazolium stimulated insulin release from β‐cells at basal glucose concentration. This effect was not mediated by protein kinase C (PKC), since it persisted in PKC‐depleted cells. R p cAMPS significantly attenuated tha calmidazolium‐stimulated insulin secretion, indicating that calmidazolium acts, at least partly, through PKA. The compound also stimulated insulin secretion from electropermeabilized β‐cells, indicating effects on distal steps in the stimulus‐secretion coupling. The use of calmidazolium offers possibilities to investigate the mechanisms activating exocytosis under conditions where the cytoplasmic‐free Ca 2+ concentration does not increase.