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• W2105165057 abstract "We investigated the role of the mitochondrial ATP-sensitive K + (K ATP ) channel, the mitochondrial big-conductance Ca 2+ -activated K + (BK Ca ) channel, and the mitochondrial permeability transition pore (MPTP) in the ouabain-induced increase of mitochondrial Ca 2+ in native rat ventricular myocytes by loading cells with rhod 2-AM. To overload mitochondrial Ca 2+ , we pretreated cells with ouabain before applying mitochondrial K ATP or BK Ca channel and/or MPTP opener. Ouabain (1 mM) increased the rhod 2-sensitive fluorescence intensity (160 ± 5.0% of control), which was dramatically decreased to the control level on application of diazoxide and NS-1619 in a dose-dependent manner (half-inhibition concentrations of 78.3 and 7.78 μM for diazoxide and NS-1619, respectively). This effect was reversed by selective inhibition of the mitochondrial K ATP channel by 5-hydroxydecanoate, the mitochondrial BK Ca channel by paxilline, and the MPTP by cyclosporin A. Although diazoxide did not efficiently reduce mitochondrial Ca 2+ during prolonged exposure to ouabain, NS-1619 reduced mitochondrial Ca 2+ . These results suggest that although mitochondrial BK Ca and K ATP channels contribute to reduction of ouabain-induced mitochondrial Ca 2+ overload, activation of the mitochondrial BK Ca channel more efficiently reduces ouabain-induced mitochondrial Ca 2+ overload in our experimental model." @default.
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• W2105165057 date "2007-07-01" @default.
• W2105165057 modified "2023-10-03" @default.
• W2105165057 title "Mitochondrial Ca²⁺-activated K⁺channels more efficiently reduce mitochondrial Ca²⁺overload in rat ventricular myocytes" @default.
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• W2105165057 doi "https://doi.org/10.1152/ajpheart.00789.2006" @default.
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