首页> 外文期刊>American Journal of Physiology >State-dependent modification of ATP-sensitive K+ channels by phosphatidylinositol 4,5-bisphosphate.
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State-dependent modification of ATP-sensitive K+ channels by phosphatidylinositol 4,5-bisphosphate.

机译:磷脂酰肌醇4,5-双磷酸酯对ATP敏感K +通道的状态依赖性修饰。

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摘要

With inside-out patch recordings in ventricular myocytes from the hearts of guinea pigs, we studied ATP-sensitive K+ (K(ATP)) channels activated by phosphatidylinositol 4,5-bisphosphate (PIP2) with respect to sensitivity to ATP when in either a rundown state (RS) or a non-rundown state (NRS). Rundown of K(ATP) channels was induced by exposure either to ATP-free solution or to ATP-free solution containing 19 microM Ca2+. Exposure of membrane patches to 10 microM PIP2 reactivated channels with both types of rundown. The reactivation by PIP2 did not require ATP in the bath. The IC50 of channels recovered from RS and before the rundown was 37.1 and 31.1 microM, respectively. PIP2 irreversibly increased the mean current when the channel was in the NRS. This was associated with a shift of IC50 to 250.6 microM after PIP2 exposure. PIP2 activates NRS K(ATP) channels by decreasing their sensitivity to ATP, whereas PIP2 reactivates RS-K(ATP) channels independently of ATP without changing ATP sensitivity.
机译:在豚鼠心脏的心室肌细胞中由内而外的补丁记录中,我们研究了磷脂酰肌醇4,5-二磷酸酯(PIP2)激活的ATP敏感K +(K(ATP))通道在两种情况下对ATP的敏感性精简状态(RS)或非精简状态(NRS)。通过暴露于不含ATP的溶液或含19 microM Ca2 +的不含ATP的溶液诱导K(ATP)通道的流失。两种类型的流失膜暴露于10 microM PIP2重新激活的通道。通过PIP2进行的重新活化在浴液中不需要ATP。从RS中恢复并在减少之前,通道的IC50分别为37.1和31.1 microM。当通道位于NRS中时,PIP2不可逆地增加了平均电流。 PIP2暴露后,这与IC50迁移至250.6 microM有关。 PIP2通过降低NRS K(ATP)通道对ATP的敏感性来激活NRS K(ATP)通道,而PIP2独立于ATP重新激活RS-K(ATP)通道而不改变ATP敏感性。

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