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 ofATPregulated 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.
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; RX871024 Induces Ca2+ Mobilization From Thapsigargin-Sensitive Stores in Mouse Pancreatic β-Cells. Diabetes 1 February 1998; 47 (2): 211–218. https://doi.org/10.2337/diab.47.2.211
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