Dissociation between exocytosis and Ca2+-channel activity in mouse pancreatic β-cells stimulated with calmidazolium (compound R24571)

Henrik Kindmark, Martin Köhler, Olof Larsson, Akhtar Khan, Per Olof Berggren

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Calmidazolium, a calmodulin inhibitor, suppressed influx of Ca2+ through voltage-gated Ca2+ 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. RpcAMPS 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 Ca2+ concentration does not increase.

Original languageEnglish (US)
Pages (from-to)315-320
Number of pages6
JournalFEBS letters
Volume369
Issue number2-3
DOIs
StatePublished - Aug 7 1995

Keywords

  • Calmidazolium
  • Insulin secretion
  • Protein kinase A
  • Voltage-gated Ca channel

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

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