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.
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
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Henrik Kindmark, Martin Köhler, Pär Gerwins, Olof Larsson, Akhtar Khan, Martin A. Wahl, Per-Olof Berggren; 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. Biosci Rep 1 June 1994; 14 (3): 145–158. doi: https://doi.org/10.1007/BF01240247
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