ATP-sensitive K(+)-channel run-down is Mg2+ dependent.

R Z Kozlowski, M L Ashford
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引用次数: 59

Abstract

ATP-sensitive K(+)-channel currents were recorded from isolated membrane patches and voltage-clamped CRI-G1 insulin-secreting cells. Internal Mg2+ ions inhibited ATP-K+ channels by a voltage-dependent block of the channel current and decrease of open-state probability. The run-down of ATP-K+ channel activity was also shown to be [Mg2+]i dependent, being almost abolished in Mg2(+)-free conditions. Substitution of Mn2+ for Mg2+ did not prevent run-down, nor did the presence of phosphate-donating nucleotides, a protease or phosphatase inhibitor or replacement of Cl- by gluconate.

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atp敏感的K(+)通道损耗依赖于Mg2+。
从分离的膜斑块和电压夹住的CRI-G1胰岛素分泌细胞中记录atp敏感的K(+)通道电流。内部Mg2+离子通过电压依赖性阻断通道电流和降低开态概率来抑制ATP-K+通道。ATP-K+通道活性的下降也被证明是[Mg2+]i依赖的,在无Mg2(+)的条件下几乎被消除。用Mn2+代替Mg2+并不能防止衰竭,磷酸提供核苷酸、蛋白酶或磷酸酶抑制剂或葡萄糖酸盐代替Cl-也不能防止衰竭。
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Proceedings of the Royal Society of London Series B-Containing Papers of Abiological Character
Proceedings of the Royal Society of London Series B-Containing Papers of Abiological Character 生命科学, 发育生物学与生殖生物学, 发育生物学
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