摘要
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。
Aim: To study modulation of protein kinase A (PKA) and protein kinase C (PKC) on the delayed rectifier potassium current ( I k )in guinea pig ventricular myocytes. Methods: The delayed rectifier potassium current was recorded by using whole cell arrangement of the patch clamp procedure. Results:cAMP 150 μmol/L increased intracellularly I k and I k,tail (pA/pF) from 13.7±2.1 and 6.1 ±0.1 to 18.5±3.3 and 6.4±2.1 ( P <0.01, n =6). I k and I k,tail (pA/pF) were augmented by 8 CPT cAMP 150 μmol/L extracellularly from 11.4±1.8 and 5.3±0.6 to 17.9±4.0 and 6.2±1.3. The half maximal voltage of activation of I k was shifted from +23.3 mV to 18.7 mV by cAMP. Phorbol 12 myristate 13 acetate(PMA, 10.0 μmol/L)applied intracellularly caused an enhance effect on I k ,with increasing I k and I k,tail (pA/pF)from 12.9±1.8 and 5.0±1.7 to 23.7±2.8 and 7.5±1.1.With shifting position potential of depolarization, effect of PMA on I k was gradually augmented. PMA resulted in shifting the slop of activation curve from +15.3 mV to +25.6 mV, with only a small effect on the half maximal voltage of activation of I k . Conclusion: I k was increased by both PKA and PKC, with different characteristics of regulation.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2002年第4期354-357,共4页
Chinese Journal of Applied Physiology
