Vascular KCNQ channels in humans: the sub-threshold brake that regulates vascular tone?
Vascular KCNQ channels in humans: the sub-threshold brake that regulates vascular tone?
复制标题
人体血管 KCNQ 通道：调节血管张力的阈下制动？
DOI：
10.1111/j.1476-5381.2010.01065.x
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发表时间：
2011
影响因子：
7.3
通讯作者：
Byron,KennethL
中科院分区：
文献类型：
--
作者：
Mani,BharathK;Byron,KennethL
动脉平滑肌细胞的收缩导致血管收缩，从而减少血流量并升高血压。人们对了解调节平滑肌收缩的离子机制非常感兴趣，部分原因是离子通道代表了针对心血管疾病和其他疾病的治疗的潜在药理学靶点。钾通道因其在维持或稳定负膜电压方面的作用而得到认可。钾通道的激活会阻碍电压敏感钙通道的打开，钙通道将钙离子传导到平滑肌细胞中以刺激收缩。最近在大鼠和小鼠的动脉平滑肌细胞中发现了 KCNQ 钾通道。这些通道具有独特的药理学和生物物理特性，使其成为膜电压的重要调节剂和调节血管收缩力的新药理学靶点。在本期《英国药理学杂志》中，Nget 等人将啮齿动物模型的研究结果扩展到人类脉管系统，并确定 KCNQ 通道也调节人类动脉的收缩。这些发现对于使用药理学 KCNQ 通道调节剂治疗人类疾病具有重要意义。链接文章本文是对本期 Nget 等人第 42-53 页的评论。要查看本文，请访问 http://dx.doi.org/10.1111/j.1476‐5381.2010.01027.x
Contraction of arterial smooth muscle cells results in vasoconstriction, which in turn reduces blood flow and increases blood pressure. There has been a great deal of interest in understanding the ionic mechanisms that regulate smooth muscle contraction, in part because ion channels represent potential pharmacological targets for therapies directed towards cardiovascular diseases and other conditions. Potassium channels have been recognized for their roles in maintaining or stabilizing negative membrane voltages. Activation of potassium channels opposes opening of voltage‐sensitive calcium channels which conduct calcium ions into the smooth muscle cells to stimulate contraction. KCNQ potassium channels were recently discovered in arterial smooth muscle cells from rats and mice. These channels have distinctive pharmacological and biophysical characteristics that have led them to be implicated as important regulators of membrane voltage and as novel pharmacological targets for modulation of vascular contractility. In this issue ofBritish Journal of Pharmacology, Nget al., extend the findings from rodent models to the human vasculature and establish that KCNQ channels also regulate constriction of human arteries. The findings have important implications for the use of pharmacological KCNQ channel modulators to treat human diseases.LINKED ARTICLEThis article is a commentary on Nget al., pp. 42–53 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476‐5381.2010.01027.x