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- W3105601446 abstract "Abstract Controversy surrounds the molecular identity of mitochondrial K + channels that are important for protection against cardiac ischemia-reperfusion injury. While K Na 1.2 ( Kcnt2 gene) is necessary for cardioprotection by volatile anesthetics, electrophysiologic evidence for a channel of this type in mitochondria is lacking. The endogenous physiologic role of a potential mito-K Na 1.2 channel is also unclear. Herein, single channel patch-clamp of 27 independent cardiac mitochondrial inner membrane (mitoplast) preparations from wild type (WT) mice yielded 6 channels matching the known ion-sensitivity, ion-selectivity, pharmacology and conductance properties of K Na 1.2 (slope conductance 138±1 pS). However, similar experiments on 40 preparations from Kcnt2 -/- mice yielded zero such channels. The K Na opener bithionol uncoupled respiration in WT but not Kcnt2 -/- cardiomyocytes. Furthermore, when oxidizing only fat as substrate, Kcnt2 -/- cardiomyocytes and hearts were less responsive to increases in energetic demand. Kcnt2 -/- mice also had elevated body fat, but no baseline differences in the cardiac metabolome. These data support the existence of a cardiac mitochondrial K Na 1.2 channel, and a role for cardiac K Na 1.2 in regulating metabolism under conditions of high energetic demand." @default.
- W3105601446 created "2020-11-23" @default.
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- W3105601446 date "2017-11-21" @default.
- W3105601446 modified "2023-10-18" @default.
- W3105601446 title "Cardiac metabolic effects of KNa1.2 channel deletion, and evidence for its mitochondrial localization" @default.
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- W3105601446 doi "https://doi.org/10.1101/223321" @default.
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