Y A Mei, L X Huang, H Wei, J T Sun, H Q Zhou, Z H Zhang
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引用次数: 0
摘要
目的:研究黄鸡胚胎心脏细胞电压依赖性外向K+电流。方法:采用全细胞膜片钳技术。结果:体外K+电流在我们细胞模内的动力学和药理学与白鸡不同。与钙激活的K+电流一样,钙通道阻滞剂CdCl2消除了95%以上的电流。异丙肾上腺素增加了细胞的峰值幅度(137% +/- 47%,n = 16个细胞),加速了细胞在外向K+电流下的活化动力学(达到峰值电流的时间从36 ms +/- 10 ms缩短到16 ms +/- 9 ms)。异丙肾上腺素的这种作用被cAMP所抑制。此外,camp诱导的磷酸化后,电流的峰值幅度出现频率依赖性下降。结论:K+通道的特性存在物种和/或细胞类型特异性差异。在胚胎黄鸡心脏细胞中,通道的磷酸化不仅可以调节钙活化钾通道的激活动力学特性,还可以改变其恢复动力学。
Characterization of outward potassium current in embryonic chick heart cells.
Aim: To characterize a voltage-dependent outward K+ current in cultured heart cells of 14-16-day-old embryos of yellow chick.
Methods: The patchclamp technique in the whole-cell configuration was used.
Results: The kinetics and the pharmacology of the outward K+ current in our cell mold were different from those described in white chick. Like the calcium-activated K+ current, blocker of calcium channel, CdCl2, eliminated the current of more than 95%. Isoproterenol provoked an increase of peak amplitude (137% +/- 47%, n = 16 cells) and acceleration of activation kinetics in the outward K+ current (the time reaching a peak current reduced from 36 ms +/- 10 ms to 16 ms +/- 9 ms). This effect of isoproterenol was mimiced by cAMP. In addition, a frequency-dependent decrease in peak amplitude of the current occurred after cAMP-induced phosphorylation.
Conclusion: There are species- and/or cell-type-specific difference in the K+ channels properties. In embryonic yellow chick heart cells, the phospholation of channel could not only modulate the activation kinetic properties of the calcium-activated potassium channel, but also change their recovery kinetics.