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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of Ba2+-resistant K+ channels in endothelium-dependent hyperpolarization of rat small mesenteric arteries.
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Role of Ba2+-resistant K+ channels in endothelium-dependent hyperpolarization of rat small mesenteric arteries.

机译：Ba2 +抵抗性K +通道在大鼠小肠系膜动脉内皮依赖性超极化中的作用。

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摘要

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.
机译：在大鼠小肠系膜动脉中，研究了调节基底平滑肌K +外排对内皮依赖性超极化机制的影响。使用常规的微电极技术测量血管平滑肌细胞的膜电位。间隙连接解偶联剂羧苄索隆（20 micro M）对静息动脉的温育可降低由最大浓度的乙酰胆碱（3 micro M）引起的内皮依赖性超极化，降至对照的约65％。在Ba2 +（200 micro M）使膜电位去极化10 mV的情况下，乙酰胆碱诱导的膜电位响应的大小增加了一倍，达到与对照无差异的值。此外，在这些条件下，超极化对羧苄酮的耐受性更高。最后，在不存在和存在羧苄索隆的情况下，Ba2 +和哇巴因（0.5 mM）的联合应用都不能消除乙酰胆碱的应答。这些结果表明，间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，超极化不依赖于向内整流的K +通道的激活。尽管不能排除钠钾泵送的微小贡献，但Ba2 +实验表明膜电响应是通过激活耐Ba2 +的K +电导介导的。

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