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目的 :研究蛋白激酶A和蛋白激酶C对豚鼠心室肌细胞延迟整流钾电流 (Ik)的影响。方法 :采用电极内液浓度差扩散法进行细胞内给药 ,利用全细胞膜片箝技术测定单细胞Ik。结果 :cAMP15 0 μmol/L使Ik及Ik ,tail(pA/pF)从 13.7± 2 .1和 6 .1± 0 .3增至 18.5± 3.3和 6 .4± 2 .1(P <0 .0 1,n =6 ) ;8 CPT cAMP15 0 μmol/L使电流 (pA/pF)从 11.4± 1.8及 5 .3± 0 .6增至 17.9± 4 .0和 6 .2± 1.3,PKA的选择性抑制剂 6 2 2 1.0 μmol/L的可逆转二者的作用。cAMP使Ik的激活曲线左移 ,半激活电压 (V1/ 2 )从 +2 3.3mV移至 +18.7mV ,激活曲线斜率 (k)在用药前后变化较小。 10 μmol/LPMA可以分别使Ik和Ik ,tial(pA/pF)从 12 .9± 1.8和 5 .0± 1.7升至 2 3.7± 2 .8和 7.5±1.1。PMA使I V曲线幅值增加 ,并随去极化电压的升高其作用加强 ,同时PMA使通道的激活曲线k从 +15 .3mV升到 +2 5 .6mV ,但对V1/ 2 基本无影响。结论 :蛋白激酶A和蛋白激酶C均可增加豚鼠心肌细胞Ik,但二者作用特点有所不同
Objective: To investigate the effects of protein kinase A and protein kinase C on delayed rectifier potassium current (Ik) in guinea pig ventricular myocytes. Methods: Intracellular drug concentration diffusion diffusion method for intracellular administration, whole cell patch clamp technique for determination of single cell Ik. Results: The levels of Ik and Ik, tail (pA / pF) increased from 13.7 ± 2.1 and 6.1 ± 0.3 to 18.5 ± 3.3 and 6.4 ± 2.1 (c <0.05) with cAMP15 0 μmol / 0 1, n = 6); 8 CPT cAMP15 0 μmol / L increased current (pA / pF) from 11.4 ± 1.8 and 5.3 ± 0.6 to 17.9 ± 4.0 and 6.2 ± 1.3, The selective inhibitor 6 2 2 1.0 μmol / L reverses the effect of both. The activation curve of Ik was left shifted to cAMP, and the half activation voltage (V1 / 2) was shifted from +2 3.3mV to + 18.7mV. The slope of activation curve (k) changed little before and after treatment. 10 μmol / LPMA increased Ik and Ik, tial (pA / pF) from 12.9 ± 1.8 and 5.0 ± 1.7 to 23.7 ± 2.8 and 7.5 ± 1.1, respectively. PMA increased the amplitude of IV curve and enhanced its effect with the increase of depolarization voltage. At the same time, PMA increased the channel activation curve k from +15 .3 mV to +25.6 mV, but had no effect on V1 / 2 . Conclusion: Both protein kinase A and protein kinase C can increase Ik in guinea pig cardiomyocytes, but their roles are different