The role of Mg2+ in the inactivation of inwardly rectifying K+ channels in aortic endothelial cells.

The role of Mg2+ in the inactivation of inwardly rectifying K+ channels in aortic endothelial cells.
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MG2+在主动脉内皮细胞中向内整流的K+通道失活中的作用。

DOI:
10.1085/jgp.105.4.463
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发表时间:
1995-04
期刊:
The Journal of general physiology
影响因子:
--
通讯作者:
Lansman JB
Lansman JB
中科院分区:
其他
文献类型:
--
作者:
Elam TR;Lansman JB

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我们研究了Mg ~(2+)在血管内皮细胞内向整流钾通道失活中的作用。失活在很大程度上消除了Mg(2+)-免费的外部解决方案和失活的程度增加,通过提高Mg(2+)。通道开放概率降低的剂量-反应关系显示Mg 2 + 0结合至感测来自外膜表面的约38%的电位降的位点(在-160 mV下KD =约25 μ M)。单通道动力学的分析表明,Mg 2+产生一类长寿命的封闭,分开的突发开口。升高Mg 2 + 0降低了爆发持续时间,但低于开放通道阻断机制的预期。Mg ~(2+)~ o的作用被K ~+~ o所拮抗,表明K ~+与Mg ~(2+)竞争失活位点。Mg ~(2+)O在毫摩尔浓度下通过快速阻断开放通道也降低了单通道电流的幅度。提出了一种机制,其中Mg 2+结合到超极化过程中的封闭通道,并防止它打开,直到它被K+占据。
We have studied the role of Mg2+ in the inactivation of inwardly rectifying K+ channels in vascular endothelial cells. Inactivation was largely eliminated in Mg(2+)-free external solutions and the extent of inactivation was increased by raising Mg2+o. The dose-response relation for the reduction of channel open probability showed that Mg2+o binds to a site (KD = approximately 25 microM at -160 mV) that senses approximately 38% of the potential drop from the external membrane surface. Analysis of the single-channel kinetics showed that Mg2+ produced a class of long-lived closures that separated bursts of openings. Raising Mg2+o reduced the burst duration, but less than expected for an open-channel blocking mechanism. The effects of Mg2+o are antagonized by K+o in manner which suggests that K+ competes with Mg2+ for the inactivation site. Mg2+o also reduced the amplitude of the single-channel current at millimolar concentrations by a rapid block of the open channel. A mechanism is proposed in which Mg2+ binds to the closed channel during hyperpolarization and prevents it from opening until it is occupied by K+.
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影响因子: --
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