RX871024 induces Ca2+ mobilization from thapsigargin-sensitive stores in mouse pancreatic β-cells

Ioulia B. Efanova, Sergei V. Zaitsev, Graham Brown, Per Olof Berggren, Suad Efendić

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

The effects of RX871024, a compound with an imidazoline structure, on cytoplasmic-free Ca2+ concentration ([Ca2+](i)) in mouse pancreatic β- cells were studied. RX871024 modulates [Ca2+](i) by at least two mechanisms. One mechanism involves closure of ATP-regulated K+ channels, resulting in membrane depolarization, opening of voltage-gated L-type Ca2+ channels, and a subsequent increase in [Ca2+](i). Another mechanism, reported here for the first time, deals with RX871024-induced mobilization of Ca2+ from nonmitochondrial thapsigargin-sensitive intracellular stores. Reduced glutathione, inhibitors of cytochrome P-450, and monoaminooxidases A and B blocked this Ca2+ mobilization. It is concluded that the mechanism of RX871024-induced Ca2+ mobilization from intracellular stores involves changes in the oxidation/reduction state of the pancreatic β-cell and may be controlled by cytochrome P-450.

Original languageEnglish (US)
Pages (from-to)211-218
Number of pages8
JournalDiabetes
Volume47
Issue number2
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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    Efanova, I. B., Zaitsev, S. V., Brown, G., Berggren, P. O., & Efendić, S. (1998). RX871024 induces Ca2+ mobilization from thapsigargin-sensitive stores in mouse pancreatic β-cells. Diabetes, 47(2), 211-218. https://doi.org/10.2337/diab.47.2.211