Evidence for, and Metabolic Consequences of, a Cardiac Mitochondrial KNa1.2 Channel

摘要: Controversy surrounds the molecular identity of mitochondrial K + channels important for protection against cardiac ischemia-reperfusion injury. While Na 1.2 ( Kcnt2 gene) is necessary cardioprotection by volatile anesthetics, electrophysiologic evidence a lacking. The endogenous physiologic role potential mito-K also unclear. Herein, single channel patch-clamp inner membranes from wild type (WT) and -/- mice yielded respectively 6/27 0/40 channels, matching known ion-sensitivity, ion-selectivity, pharmacology conductance properties (WT slope 138±1 pS). opener bithionol uncoupled respiration in WT but not cardiomyocytes. Furthermore, when oxidizing only fat as substrate, cardiomyocytes hearts were less responsive to increases energetic demand. had elevated body fat, no baseline differences metabolome. These data support existence with metabolic regulatory under high