The imidazoline derivative calmidazolium inhibits voltage-gated Ca2+-channels and insulin release but has no effect on the phospholipase C system in insulin producing RINm5F-cells

Henrik Kindmark, Martin Köhler, Pär Gerwins, Olof Larsson, Akhtar Khan, Martin A. Wahl, Per Olof Berggren

Research output: Contribution to journalArticle

10 Scopus citations


The present study shows that the calmodulin antagonist calmidazolium inhibited influx of Ca2+ through voltage-gated Ca2+-channels in clonal insulin producing RINm5F-cells. The mechanism of inhibition may involve both Ca2+-calmodulin-dependent protein kinases and direct binding of calmidazolium to the Ca2+-channel. Calmidazolium did not affect uptake of Ca2+ into intracellular Ca2+-pools, inositol 1,4,5-trisphosphate (InsP3) formation or action on intracellular Ca2+-pools. The calmodulin inhibitor also did not affect glucose utilization or oxidation in RINm5F-cells, speaking against an unspecific toxic effect of the compound. KCl-and ATP-stimulated insulin release from RINm5F-cells was attenuated by calmidazolium, whereas basal hormone secretion was unaffected.

Original languageEnglish (US)
Pages (from-to)145-158
Number of pages14
JournalBioscience reports
Issue number3
StatePublished - Jun 1 1994



  • Ca-channels
  • calmidazolium
  • calmodulin inhibitor
  • insulin release
  • RINm5F-cells

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry, Genetics and Molecular Biology(all)

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