Ion channels in vascular smooth muscle cells control membrane potential, which is a major determinant of the intracellular Ca2+ concentration and thus vascular tone. Membrane potential is modulated by a complex collection of endogenous vasodilator and vasoconstrictor pathways that ultimately dictate regional vascular resistance, organ blood flow, and systemic arterial pressure. Membrane potential in vascular smooth muscle is dominated by multiple types of K+ channels including those regulated by Ca2+, voltage, and ATP.1 It is not surprising then that K+ channels in vascular smooth muscle have been studied extensively as targets in normal vasoregulatory pathways and as end-effectors gone awry in diseases. Most investigations to date have focused on traditional intracellular signaling systems (eg, cyclic nucleotides and their associated kinases2) and chronic changes in expression patterns (eg, downregulation of subunits3). Article, see p 650 In the present issue of Circulation Research , Zhai et al4 examine the novel hypothesis that endothelin-1 elicits vasoconstriction, in part, by rapidly altering the subunit composition of vascular smooth muscle K+ channels, thereby reducing their functional activity. The K+ channel under investigation is the large conductance Ca2+-activated K+ channel, known colloquially as BK (K+ channels of big conductance).1 The subunit composition of BK …

中文翻译：

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平滑肌中BK通道亚基组成的动态调节

血管平滑肌细胞中的离子通道控制膜电位，这是细胞内Ca2 +浓度和血管张力的主要决定因素。膜电位是由内源性血管扩张剂和血管收缩剂通路的复杂集合调节的，这些通路最终决定了区域性血管阻力，器官血流和全身动脉压。血管平滑肌的膜电位受多种类型的K +通道支配，包括受Ca2 +，电压和ATP调节的K +通道。[1]因此，对血管平滑肌中的K +通道作为正常血管调节途径的靶点和靶点进行广泛研究就不足为奇了。终端执行者在疾病中出了问题。迄今为止，大多数研究都集中在传统的细胞内信号系统（例如，环核苷酸及其相关的激酶2）和表达模式的慢性变化（例如，亚基的下调3）。文章，请参阅第650页。在本期《循环研究》中，Zhai等[4]研究了一种新的假设，即内皮素-1会部分地通过迅速改变血管平滑肌K +通道的亚基组成，从而降低其功能活性而引起血管收缩。研究中的K +通道是大电导的Ca2 +激活的K +通道，俗称BK（大电导的K +通道）。1BK的亚基组成… 通过迅速改变血管平滑肌K +通道的亚基组成，从而降低其功能活性。研究中的K +通道是大电导的Ca2 +激活的K +通道，俗称BK（大电导的K +通道）。1BK的亚基组成… 通过迅速改变血管平滑肌K +通道的亚基组成，从而降低其功能活性。研究中的K +通道是大电导的Ca2 +激活的K +通道，俗称BK（大电导的K +通道）。1BK的亚基组成…