ATP-SENSITIVE K+ CHANNELS IN RAT VENTRICULAR MYOCYTES ARE BLOCKED AND INACTIVATED BY INTERNAL DIVALENT-CATIONS
ATP-SENSITIVE K+ CHANNELS IN RAT VENTRICULAR MYOCYTES ARE BLOCKED AND INACTIVATED BY INTERNAL DIVALENT-CATIONS
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DOI：
10.1007/bf00580282
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发表时间：
1987-10-01
影响因子：
4.5
通讯作者：
FINDLAY, I
中科院分区：
文献类型：
--
作者：
FINDLAY, I
从离体大鼠心室肌细胞的内向外斑块中的 ATP 敏感通道记录 K+ 电流。在不存在内部二价阳离子的情况下，电流电压关系可以通过渗透率为 1.25 倍的恒定场假设来描述。 10-113平方厘米/秒；外向电流饱和，为 K+ 运动提供高驱动力。内部0.1-5.0mM Mg2+、0.1μM Ca2+和10mM Na+各自抑制K+离子通过开放通道向外移动的通量。内部 0.1-5.0 mM Mg2+、0.1-1.0 μM Ca2+ 和 1-10 μM Ba2+ 和 Sr2+ 以剂量和电压依赖性方式阻断 K+ 通道活性。耗尽的通道可以被 Mg-ATP 重新激活，但不能被 AMP-PNP、ATP.gamma.S 或无 Mg 的 ATP 重新激活，这表明通道的磷酸化与其活性有关。 Ca 2+ (> = 1 μM)和Sr 2+ (1 mM)显着灭活K+ ATP通道，毫摩尔Ba 2+ 或Mg 2+ 效果较差。这表明通道的耗尽是 K+ 通道蛋白的 Ca2+ 依赖性去磷酸化。
K+ currents were recorded from ATP-sensitive channels in inside-out patches from isolated rat ventricular myocytes. In the absence of internal divalent cations the current voltage relationship could be described by constant-field assumptions with a permeability of 1.25 .times. 10-113 cm2/s; outward currents saturated udner a high driving force for K+ movement. Internal 0.1-5.0mM Mg2+, 0.1 .mu.M Ca2+ and 10 mM Na+ each depressed the flux of K+ ions moving outwards through open channels. Internal 0.1-5.0 mM Mg2+, 0.1-1.0 .mu.M Ca2+ and 1-10 .mu.M Ba2+ and Sr2+ blocked K+ channel activity in a dose- and voltage-dependent manner. Run-down channels could be reactivated by Mg-ATP, but not by AMP-PNP, ATP.gamma.S or Mg-free ATP which suggested that phosphorylation of the channels was involved in their activity. Ca2+ (> = 1 .mu.M) and Sr2+ (1 mM) markedly inactivated K+ ATP channels, millimolar Ba2+ or Mg2+ were less effective. This suggested that the run down of the channels was a Ca2+-dependent dephosphorylation of the K+ channel protein.