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钡离子抗性钾通道在大鼠小肠系膜动脉内皮依赖性超极化中的作用。

Role of Ba2+-resistant K+ channels in endothelium-dependent hyperpolarization of rat small mesenteric arteries.

作者信息

Breyne Joke, Vanheel Bert J

机构信息

Department of Physiology and Physiopathology, Ghent University, U.G.-UZ, Blok B, De Pintelaan 185, B-9000 Ghent, Belgium.

出版信息

Can J Physiol Pharmacol. 2004 Jan;82(1):65-71. doi: 10.1139/y03-132.

DOI:10.1139/y03-132
PMID:15052307
Abstract

In rat small mesenteric arteries, the influence of modulation of basal smooth muscle K+ efflux on the mechanism of endothelium-dependent hyperpolarization was investigated. The membrane potentials of the vascular smooth muscle cells were measured using conventional microelectrode techniques. Incubation of resting arteries with the gap junction uncoupler carbenoxolone (20 micro M) decreased the endothelium-dependent hyperpolarization elicited by a submaximal concentration of acetylcholine (3 micro M) to about 65% of the control. In the presence of Ba2+ (200 micro M), which depolarized the membrane potential by 10 mV, the acetylcholine-induced membrane potential response was doubled in magnitude, reaching values not different from control. Moreover, the hyperpolarization was more resistant to carbenoxolone in these conditions. Finally, both in the absence and in the presence of carbenoxolone, the combined application of Ba2+ and ouabain (0.5 mM) did not abolish the acetylcholine response. These results suggest that gap junctional coupling plays a role in endothelium-dependent hyperpolarization of smooth muscle cells of resting rat small mesenteric arteries. Additionally, these findings show that the hyperpolarization does not rely on activation of inward rectifying K+ channels. Although a minor contribution of Na-K pumping cannot be excluded, the Ba2+ experiments show that the membrane electrical response is mediated by activation of a Ba2+-resistant K+ conductance.

摘要

在大鼠小肠系膜动脉中,研究了基础平滑肌钾离子外流调节对内皮依赖性超极化机制的影响。使用传统微电极技术测量血管平滑肌细胞的膜电位。用缝隙连接解偶联剂羧苄青霉素(20微摩尔)孵育静息动脉,可使亚最大浓度乙酰胆碱(3微摩尔)引起的内皮依赖性超极化降低至对照的约65%。在存在钡离子(200微摩尔)的情况下,膜电位去极化10毫伏,乙酰胆碱诱导的膜电位反应幅度加倍,达到与对照无差异的值。此外,在这些条件下,超极化对羧苄青霉素更具抗性。最后,无论是否存在羧苄青霉素,钡离子和哇巴因(0.5毫摩尔)联合应用均未消除乙酰胆碱反应。这些结果表明,缝隙连接偶联在静息大鼠小肠系膜动脉平滑肌细胞的内皮依赖性超极化中起作用。此外,这些发现表明超极化不依赖于内向整流钾通道的激活。虽然不能排除钠钾泵的微小贡献,但钡离子实验表明膜电反应是由对钡离子有抗性的钾离子电导激活介导的。

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