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大鼠心室肌细胞ATP敏感性钾通道的钙依赖性失活

Calcium-dependent inactivation of the ATP-sensitive K+ channel of rat ventricular myocytes.

作者信息

Findlay I

机构信息

Laboratoire de Physiologie Comparée, (UA CNRS 1121), Université de Paris XI, Orsay, France.

出版信息

Biochim Biophys Acta. 1988 Aug 18;943(2):297-304. doi: 10.1016/0005-2736(88)90561-5.

Abstract

Single-channel currents were recorded from ATP-sensitive K+ channels in inside-out membrane patches excised from isolated rat ventricular myocytes. Perfusion of the internal surface of excised membrane patches with solutions which contained between 5 and 100 microM free calcium caused the loss of K+ATP channel activity which was not reversed when the membranes were washed with Ca-free solution. K+ATP channel activity could be recovered by bathing the patches in Mg.ATP. The loss of K+ATP channel activity provoked by internal calcium was a process which occurred over a time scale of seconds. Channel closure evoked by internal ATP was essentially instantaneous. The speed of K+ATP channel inactivation increased with the concentration of calcium. Neither a phosphatase inhibitor (fluoride ions) nor a proteinase inhibitor (leupeptin) had any effect upon the loss of K+ channel activity stimulated by internal calcium.

摘要

从分离的大鼠心室肌细胞中切除的内向外膜片中记录了ATP敏感性钾通道的单通道电流。用含有5至100微摩尔游离钙的溶液灌注切除膜片的内表面,导致钾ATP通道活性丧失,当用无钙溶液洗涤膜片时,这种丧失并未逆转。钾ATP通道活性可通过将膜片置于Mg.ATP中恢复。内部钙引起的钾ATP通道活性丧失是一个在数秒时间尺度上发生的过程。内部ATP引起的通道关闭基本上是瞬间的。钾ATP通道失活的速度随钙浓度增加而加快。磷酸酶抑制剂(氟离子)和蛋白酶抑制剂(亮抑酶肽)对内部钙刺激引起的钾通道活性丧失均无任何影响。

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