Sakai R, Hagiwara N, Kasanuki H, Hosoda S
Heart Institute of Japan, Tokyo Women's Medical College, Japan.
J Mol Cell Cardiol. 1995 Oct;27(10):2403-8. doi: 10.1016/s0022-2828(95)92199-0.
Many types of chloride current have been reported in the hearts of various species; however, the nature of chloride conductance in the human heart is still unclear. We investigated cyclic AMP-dependent chloride current and swelling-induced chloride current in isolated human atrial cells using the whole-cell voltage-clamp method. External application of 1 microM isoprenaline increased calcium current by 391.9 +/- 48.6% (mean +/- S.D., n = 8); however, there was no activation of cyclic AMP-dependent chloride current at steady-state membrane potentials between -80 and +50 mV. Neither external application of 10 microM forskolin nor internal application of 50 microM cyclic AMP activated a cyclic AMP-dependent chloride current. On the other hand, when the same cell was superfused with a 50% hypotonic solution, it exhibited osmotic swelling and an outward rectifying current (6.59 +/- 0.96 pA/pF at +30 mV, n = 10). This swelling-induced current reversed at -26.5 +/- 3.1 mV (n = 10), close to the calculated equilibrium potential for chloride, and it was sensitive to the stilbene-derivative chloride channel blocker. In conclusion, no activation of cyclic AMP-dependent chloride current was observed in human atrial cells. On the other hand, a swelling-induced chloride current was consistently demonstrated and its kinetic properties were similar to those reported in other cardiac myocytes.
在各种物种的心脏中已报道了多种类型的氯电流;然而,人类心脏中氯电导的性质仍不清楚。我们使用全细胞膜片钳方法研究了分离的人心房细胞中环磷酸腺苷(cAMP)依赖性氯电流和肿胀诱导的氯电流。外部施加1微摩尔异丙肾上腺素使钙电流增加了391.9±48.6%(平均值±标准差,n = 8);然而,在-80至+50毫伏的稳态膜电位下,cAMP依赖性氯电流未被激活。外部施加10微摩尔福斯高林或内部施加50微摩尔cAMP均未激活cAMP依赖性氯电流。另一方面,当用50%的低渗溶液对同一细胞进行灌流时,它表现出渗透性肿胀和外向整流电流(在+30毫伏时为6.59±0.96皮安/皮法,n = 10)。这种肿胀诱导的电流在-26.5±3.1毫伏时反转(n = 10),接近计算出的氯平衡电位,并且它对二苯乙烯衍生物氯通道阻滞剂敏感。总之,在人心房细胞中未观察到cAMP依赖性氯电流的激活。另一方面,持续证明了肿胀诱导的氯电流,其动力学特性与其他心肌细胞中报道的相似。