Kochetkov K V, Kazachenko V N, Marinov B S
Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region.
Membr Cell Biol. 2000;14(2):285-98.
Using the patch-clamp technique in an inside-out configuration, we studied the action of an antiinflammatory drug, flufenamic acid (FFA), on single large-conductance Ca2+-activated K+ channels in cultured Vero kidney cells. Depending on its concentration, FFA caused either potentiation or inhibition of K(Ca) channel activity of the same channel. Within the concentration ranges of about 5 to 10 microM and of 50 to 500 microM, FFA increased the channel activity; and within the intermediate range of about 10 to 50 microM, FFA inhibited the channels. The effects were only partially reversible. The activating phases were accompanied by an increase in the channel open time and decreases in the channel closed time and slope factor of the Ca2+ concentration-response curve. An apparent dissociation constant of Ca2+ interaction with the channel changed slightly. Possible mechanisms of the FFA effects are discussed.
采用内面向外式膜片钳技术，我们研究了一种抗炎药物氟芬那酸（FFA）对培养的非洲绿猴肾（Vero）细胞中单个大电导钙激活钾通道的作用。根据其浓度不同，FFA对同一通道的钾钙通道活性可产生增强或抑制作用。在约5至10微摩尔以及50至500微摩尔的浓度范围内，FFA增强通道活性；而在约10至50微摩尔的中间浓度范围内，FFA抑制通道活性。这些效应只是部分可逆的。激活阶段伴随着通道开放时间增加以及通道关闭时间和钙浓度-反应曲线斜率因子减小。钙与通道相互作用的表观解离常数略有变化。文中讨论了FFA作用的可能机制。
