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• W2155381489 abstract "Abstract Acute hypoxia modulates various cell processes, such as cell excitability, through the regulation of ion channel activity. Given the central role of Ca 2+ signaling in the physiological functioning of astrocytes, we have investigated how acute hypoxia regulates such signaling, and compared results with those evoked by bradykinin (BK), an agonist whose ability to liberate Ca 2+ from intracellular stores is well documented. In Ca 2+ ‐free perfusate, BK evoked rises of [Ca 2+ ] i in all cells examined. Hypoxia produced smaller rises of [Ca 2+ ] i in most cells, but always suppressed subsequent rises of [Ca 2+ ] i induced by BK. Thapsigargin pre‐treatment of cells prevented any rise of [Ca 2+ ] i evoked by either BK or hypoxia. Restoration of Ca 2+ to the perfusate following a period of acute hypoxia always evoked capacitative Ca 2+ entry. During mitochondrial inhibition (due to exposure to carbonyl cyanide p–trifluromethoxyphenyl hydrazone (FCCP) and oligomycin), rises in [Ca 2+ ] i (observed in Ca 2+ ‐free perfusate) evoked by hypoxia or by BK, were significantly enhanced, and hypoxia always evoked responses. Our data indicate that hypoxia triggers Ca 2+ release from endoplasmic reticulum stores, efficiently buffered by mitochondria. Such liberation of Ca 2+ is sufficient to trigger capacitative Ca 2+ entry. These findings indicate that the local O 2 level is a key determinant of astrocyte Ca 2+ signaling, likely modulating Ca 2+ ‐dependent astrocyte functions in the central nervous system. © 2004 Wiley‐Liss, Inc." @default.
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• W2155381489 date "2004-07-06" @default.
• W2155381489 modified "2023-10-13" @default.
• W2155381489 title "Hypoxic regulation of Ca2+ signaling in cultured rat astrocytes" @default.
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• W2155381489 doi "https://doi.org/10.1002/glia.20083" @default.
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