Alternations of Transient Outward K<SUP>+</SUP> Current (I<SUB>to</SUB>) in Type 2 Diabetic Ventricular Cardiomyocytes
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概要
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<B>Background:</B> Although cardiac ion channel remodeling has been reported in type 1 diabetes mellitus (T1DM), modification of the channels by type 2 DM (T2DM) is poorly understood. Here we characterized ion channel properties in cardiomyocytes of OLETF, a rat model of obese T2DM. <B>Methods and Results:</B> We isolated myocytes from subepicardial (EPI) and subendocardial (END) regions of the left ventricle for whole-cell patch clamp experiments. Action potential duration at 50% repolarization (APD<SUB>50</SUB>) at 1 Hz was significantly longer in OLETF than in non-diabetic control (LETO) (EPI; 8.89±1.04 vs. 5.20±0.75 ms, END; 22.01±3.64 vs. 9.89±1.74 ms). In both EPI and END, L-type Ca<SUP>2+</SUP> current and inward rectifier K<SUP>+</SUP> current were similar between OLETF and LETO. In EPI, transient outward K<SUP>+</SUP> current (I<SUB>to</SUB>) density at 0.1 Hz was similar. However, the fast recovering component from inactivation of I<SUB>to</SUB> was significantly decreased in OLETF. In END, I<SUB>to</SUB> density at 0.1 Hz was significantly reduced in OLETF (8.77±0.78 vs. 14.50±1.31 pA/pF at +60 mV), in addition to slower recovery of I<SUB>to</SUB>. Membrane capacitances were similar in all groups. <B>Conclusions:</B> T2DM slowed I<SUB>to</SUB> recovery form inactivation and decreased END-I<SUB>to</SUB> density without cardiomyocyte hypertrophy. This regional difference in the effect on I<SUB>to</SUB> has not been reported for T1DM and appears characteristic to T2DM.
著者
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Tohse Noritsugu
Department Of Cellular Physiology And Signal Transduction Sapporo Medical University School Of Medic
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Miura Tetsuji
Second Department Of Internal Medicine Department Of Clinical Laboratory Medicine Sapporo Medical Un
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Kobayashi Takeshi
Department Of Biological Chemistry College Of Bioscience And Biotechnology Chubu University
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Sato Tatsuya
Department Of Biology Tokyo Gakugei University
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Sato Tatsuya
Department of Cellular Physiology and Signal Transduction, Sapporo Medical University
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KOBAYASHI Takeshi
Department of Cellular Physiology and Signal Transduction, Sapporo Medical University
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