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二氮嗪对胰岛素分泌细胞系记录的ATP-K+电流的双重作用。

Dual effects of diazoxide on ATP-K+ currents recorded from an insulin-secreting cell line.

作者信息

Kozlowski R Z, Hales C N, Ashford M L

机构信息

Department of Pharmacology, University of Cambridge.

出版信息

Br J Pharmacol. 1989 Aug;97(4):1039-50. doi: 10.1111/j.1476-5381.1989.tb12560.x.

Abstract
  1. The effects of diazoxide on ATP-K+ channel currents, recorded from the insulin-secreting cell line, CRI-G1, were studied using patch-clamp techniques. 2. Under current-clamp recording conditions diazoxide (0.6 mM), inhibited action potential activity and hyperpolarized CRI-G1 cells with a concomitant increase in membrane conductance. Recordings from voltage-clamped whole-cells and isolated patches indicate that activation of ATP-K+ channel currents underlie these effects. 3. Diazoxide elicited an activation of ATP-K+ channels which had been partially inhibited by ATP, on application to either surface of the plasma membrane, although it was more effective when applied directly to the cytoplasmic side. Activation of the ATP-K+ currents involves an increase in the single channel open-state probability and an apparent increase in the number of functional channels. 4. Activation was observed only when Mg-ATP was present in the cytoplasmic bathing solution. There was no activation of currents by diazoxide when ATP, in the absence of Mg2+ ions, or Mg-AMP-PNP was present to inhibit the ATP-K+ channels. 5. In the absence of ATP and Mg2+ ions in the cytoplasmic bathing solution, diazoxide (0.6 mM) produced an inhibition of ATP-K+ currents. 6. Cromakalim (BRL 34915) at 10 microM and 100 microM had no significant effects on ATP-K+ currents. 7. It is concluded that diazoxide-induced activation of ATP-K+ channel currents probably involves phosphorylation of the channel or some closely associated membrane protein.
摘要
  1. 运用膜片钳技术研究了二氮嗪对胰岛素分泌细胞系CRI-G1中ATP-K⁺通道电流的影响。2. 在电流钳记录条件下,二氮嗪(0.6 mM)抑制动作电位活性并使CRI-G1细胞超极化,同时膜电导增加。电压钳全细胞和分离膜片的记录表明,ATP-K⁺通道电流的激活是这些效应的基础。3. 二氮嗪可激活已被ATP部分抑制的ATP-K⁺通道,无论作用于质膜的哪一侧,尽管直接作用于细胞质侧时更有效。ATP-K⁺电流的激活涉及单通道开放状态概率的增加和功能通道数量的明显增加。4. 仅当细胞质灌流液中存在Mg-ATP时才观察到激活。当存在ATP(无Mg²⁺离子)或Mg-AMP-PNP以抑制ATP-K⁺通道时,二氮嗪不会激活电流。5. 在细胞质灌流液中不存在ATP和Mg²⁺离子时,二氮嗪(0.6 mM)会抑制ATP-K⁺电流。6. 10 μM和100 μM的克罗卡林(BRL 34915)对ATP-K⁺电流无显著影响。7. 得出的结论是,二氮嗪诱导的ATP-K⁺通道电流激活可能涉及通道或某些紧密相关膜蛋白的磷酸化。

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