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

FEBS Letters

Köhler, Martin¹  Berggren, Per-Olof¹  Kindmark, Henrik¹  Larsson, Olof¹  Khan, Akhtar¹ 

[1] Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institute, Karolinska Hospital, S-171 76 Stockholm, Sweden

关键词: Voltage-gated Ca2+ channel;    Calmidazolium;    Insulin secretion;    Protein kinase A;   

DOI  :  10.1016/0014-5793(95)00774-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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. R_pcAMPS 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.

【 授权许可】

Unknown