Modulation of the BK channel by estrogens: examination at single channel level
Modulation of the BK channel by estrogens: examination at single channel level
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DOI：
10.1080/09687860600802803
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发表时间：
2006-09-01
影响因子：
--
通讯作者：
Callaghan, Richard
中科院分区：
文献类型：
--
作者：
De Wet, Heidi;Allen, Marcus;Callaghan, Richard
BK 通道通过响应钙浓度波动而使平滑肌超极化来调节血管张力。据报道，雌激素通过直接结合与通道相关的调节性 β1 亚基来增加 BK 通道开放概率，从而降低血压。目前的研究表明，17β-雌二醇通过增加通道开放的突发持续时间来激活 BK 通道复合物。添加 17 β-雌二醇后，在 25% 的记录中观察到亚电导状态，这可以反映成孔 β 1 亚基和调节 β 1 亚基之间的解偶联。我们还提供了证据表明需要多个 β1 亚基来促进 17β-雌二醇与通道复合物的结合。
BK channels regulate vascular tone by hyperpolarizing smooth muscle in response to fluctuating calcium concentrations. Oestrogen has been reported to lower blood pressure by increasing BK channel open probability through direct binding to the regulatory beta 1-subunit(s) associated with the channel. The present investigation demonstrates that 17 beta-oestradiol activates the BK channel complex by increasing the burst duration of channel openings. A subconductance state was observed in 25% of recordings following the addition of 17 beta-oestradiol and could reflect uncoupling between the pore forming beta 1-subunit and the regulatory beta 1-subunit. We also present evidence that more than one beta 1-subunit is required to facilitate binding of 17 beta- oestradiol to the channel complex.