Large conductance, Ca2+-activated K+ channels (BKCa) and arteriolar myogenic signaling.
Large conductance, Ca2+-activated K+ channels (BKCa) and arteriolar myogenic signaling.
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DOI：
10.1016/j.febslet.2010.02.045
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发表时间：
2010-05-17
期刊：
影响因子：
3.5
通讯作者：
Braun AP
中科院分区：
文献类型：
--
作者：
Hill MA;Yang Y;Ella SR;Davis MJ;Braun AP
肌源性或压力诱导的血管收缩对局部血流自动调节至关重要。这种VSM反应背后的事件包括膜去极化，Ca2+进入和动员，以及收缩蛋白的激活。BKCa参与了其中的几个步骤，包括：1)通道关闭导致膜去极化，2)通道打开导致超极化，以对抗过度压力诱导的血管收缩。由于多种机制调节BKCa活性，（亚基组成，Em和Ca2+水平，翻译后修饰）组织水平的多样性被预测。重要的是，异质性可能会导致肌源性血管收缩调节的组织特异性差异，从而使局部血流动力学与代谢需求相匹配。了解这种变异性对于利用BKCa通道作为治疗靶点和理解其药理学操作的全身效应非常重要。
Myogenic, or pressure-induced, vasoconstriction is critical for local blood flow autoregulation. Underlying this VSM response are events including membrane depolarization, Ca2+ entry and mobilization, and activation of contractile proteins. BKCa has been implicated in several of these steps including, 1) channel closure causing membrane depolarization, and 2) channel opening causing hyperpolarization to oppose excessive pressure-induced vasoconstriction. As multiple mechanisms regulate BKCa activity, (subunit composition, Em and Ca2+ levels, post-translational modification) tissue level diversity is predicted. Importantly, heterogeneity may contribute to tissue-specific differences in regulation of myogenic vasoconstriction, allowing local hemodynamics to be matched to metabolic requirements. Knowledge of such variability will be important to exploiting the BKCa channel as a therapeutic target and understanding systemic effects of its pharmacological manipulation.
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DOI：
10.1085/jgp.109.5.647
发表时间：
1997-05
期刊：
The Journal of general physiology
影响因子：
--
作者：
Cui J;Cox DH;Aldrich RW
通讯作者：
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影响因子：
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4.8
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影响因子：
64.8
作者：
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影响因子：
4.8
作者：
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