Mg^(2+)对豚鼠心室肌细胞ATP敏感钾电流的抑制作用

INHIBITORY EFFECT OF EXTRACELLULAR MAGNESIUM ON ATP-SENSITIVE POTASSIUM CURRENT IN GUINEA-PIG VENTRICULAR CELLS

利用全细胞电压钳方法研究了细胞外高Mg^(2+)对豚鼠心室肌细胞I_(k,ATP)(ATP敏感钾电流)的作用。细胞的I_(k,ATP)是被代谢抑制剂2,4-二硝基酚(DNP)激活的,可被特异性阻断剂优降糖完全阻断。细胞外8mmol/L MgSO_4几乎能完全抑制DNP激活的I_(k,ATP)膜电位0mV水平时抑制率为92±8.6％;4mmol/L MgSO_4可部分抑制I_(k,ATP),抑制率为44±14.6％。Mg^(2+)与ATP联合使用对I_(k,ATP)的作用与Mg^(2+)单独作用无明显差异。结果提示,抑制I_(k,ATP)是Mg^(2+)防止缺氧或缺血状态下心肌细胞动作电位时程缩短的一个重要原因,因而可能也是Mg^(2+)抗缺血性心律失常的重要机制。

The effects of extracellular magnesium on ATP-sensitive potassium current (IK.ATP) were assessed using whole cell recording method in guinea-pig ventricular cells. With ramp voltage clamp mode, 2,4-dinitrophenol (DNP, 50 μmol / L) induced a distinct outward current. It was complete- ly abolished by application of glibenclamide, a specific blocker of IK,ATP, indicating that this current was carried through the IK,ATP channels. The IK,ATP induced by DNP was inhibited when magnesium concentration in perfusion solution increased. High concentration of magnesium reduced IK.ATP values at membrane potential 0 mV by 92 ± 8.6% (8 mmol/ L) and 44 ± 14.6% (4 mmol / L). Combined application of magnesium with ATP (0.3 mmol / L) did not enhance the effect of magnesium on IK ATP. The results suggest that inhibitory effect of magnesium on IK,ATP is a suitable explanation for magnesium to prevent shortening of action potential duration during acute myocardial hypoxia or ischemia and might be an important mechanism responsible for the antiarrhythmic effect of magnesium on acute myocardial infarction.