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成年大鼠离体心房肌细胞中一种新型的去极化激活钾电流。

A novel type of depolarization-activated K+ current in isolated adult rat atrial myocytes.

作者信息

Boyle W A, Nerbonne J M

机构信息

Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.

出版信息

Am J Physiol. 1991 Apr;260(4 Pt 2):H1236-47. doi: 10.1152/ajpheart.1991.260.4.H1236.

Abstract

To determine the types of voltage-gated K+ channels controlling action potential repolarization in atrial cells, we have characterized the properties of depolarization-activated K+ channels in isolated adult rat atrial myocytes using the whole cell patch-clamp recording technique. On membrane depolarization, Ca2(+)-independent outward K+ currents in these cells begin to activate at approximately -40mV. At all test potentials, the currents activate rapidly after a delay, and there is little or no decay of the peak outward current amplitude during brief (100 ms) depolarizations. In addition, the currents show little steady-state inactivation at membrane potentials negative to -60 mV. The currents are blocked effectively by 1-5 mM 4-aminopyridine but are relatively insensitive to extracellular tetraethylammonium at concentrations up to 50 mM. Based on the measured time- and voltage-dependent properties and the pharmacological sensitivity of the currents, we suggest that the depolarization-activated K+ channels underlying the macroscopic currents in adult rat atrial myocytes are distinct from those described previously in other myocardial preparations, including adult rat ventricular myocytes. Interestingly, the outward K+ currents characterized here in isolated adult rat atrial myocytes are remarkably similar to those of several recently described "delayed rectifier" K+ channel genes isolated from rat brain cDNA libraries and expressed in Xenopus oocytes, suggesting that similar K+ currents are likely present in cells of the mammalian central nervous system.

摘要

为了确定控制心房细胞动作电位复极化的电压门控钾通道类型,我们使用全细胞膜片钳记录技术对成年大鼠离体心房肌细胞中去极化激活的钾通道特性进行了表征。在膜去极化时,这些细胞中不依赖Ca2+的外向钾电流在约-40mV时开始激活。在所有测试电位下,电流在延迟后迅速激活,并且在短暂(100ms)去极化期间,外向电流峰值幅度几乎没有衰减或没有衰减。此外,在膜电位负于-60mV时,电流几乎没有稳态失活。这些电流可被1-5mM 4-氨基吡啶有效阻断,但对浓度高达50mM的细胞外四乙铵相对不敏感。根据测量的时间和电压依赖性特性以及电流的药理学敏感性,我们认为成年大鼠心房肌细胞中宏观电流所依赖的去极化激活钾通道与先前在其他心肌制剂(包括成年大鼠心室肌细胞)中描述的通道不同。有趣的是,这里在成年大鼠离体心房肌细胞中表征的外向钾电流与最近从大鼠脑cDNA文库中分离并在非洲爪蟾卵母细胞中表达的几种“延迟整流”钾通道基因的电流非常相似,这表明在哺乳动物中枢神经系统的细胞中可能存在类似的钾电流。

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