Piao Lin, Ho Won-Kyung, Earm Yung E
National Research Laboratory for Cellular Signalling and Department of Physiology, Seoul National University College of Medicine, 28 Yonkeun-Dong, Chongno-Ku, 110-799 Seoul, Korea.
Pflugers Arch. 2003 Aug;446(5):523-8. doi: 10.1007/s00424-003-1079-y. Epub 2003 May 13.
Using the inside-out patch-clamp technique, large-conductance Ca2+ -activated K+ channel (BK(Ca)) currents were recorded from coronary artery smooth muscle cells. Cytochalasin D, an actin filament disrupter, increased channel activity ( NP(o), where N is the number of channels and P(o) the open probability), and this increase was reversed by phalloidin, an actin filament stabilizer. NP(o) was also increased by colchicine, a microtubule disrupter, and decreased by taxol, a microtubule stabilizer. With the stepwise increase of negative pressure in the patch pipettes, the activity of BK(Ca) gradually increased: the maximum effect (527% increase in NP(o)) was achieved at -40 cmH(2)O and the half-maximum effect at -25 cmH(2)O. The increase in NP(o) in response to negative pressure was abolished by phalloidin but not by taxol. These results imply that both actin filaments and microtubules inhibit the opening of BK(Ca) in coronary artery smooth muscle cells, but that only actin filaments are involved in the stretch sensitivity of BK(Ca).
采用内面向外膜片钳技术，从冠状动脉平滑肌细胞记录大电导钙激活钾通道（BK(Ca)）电流。细胞松弛素D，一种肌动蛋白丝破坏剂，增加了通道活性（NP(o)，其中N是通道数量，P(o)是开放概率），而这种增加被鬼笔环肽，一种肌动蛋白丝稳定剂所逆转。NP(o)也被秋水仙碱，一种微管破坏剂增加，并被紫杉醇，一种微管稳定剂降低。随着膜片吸管中负压的逐步增加，BK(Ca)的活性逐渐增加：在-40 cmH(2)O时达到最大效应（NP(o)增加527%），在-25 cmH(2)O时达到半最大效应。鬼笔环肽消除了对负压响应的NP(o)增加，但紫杉醇没有。这些结果表明，肌动蛋白丝和微管都抑制冠状动脉平滑肌细胞中BK(Ca)的开放，但只有肌动蛋白丝参与BK(Ca)的拉伸敏感性。
