Ito H, Nakajima T, Takikawa R, Hamada E, Iguchi M, Sugimoto T, Kurachi Y
2nd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1991 Jul;344(1):133-6. doi: 10.1007/BF00167394.
The effect of coenzyme Q10 (CoQ10) on the cyanide (CN-)-induced ATP-sensitive K+ channel current (KATP) was examined in single atrial myocytes, using the patch clamp technique. Superfusion of the cells with a CN-/low glucose bathing solution induced an outward current in the whole-cell clamp condition. Glibenclamide (1 microM) abolished this current, indicating that the current was carried through the KATP channel. After steady-state activation by CN-, pinacidil (a KATP channel opener, 300 microM) failed to further increase the current. In cell-attached patches, CN-, when applied to the bath, induced bursting openings of an 80 pS channel (the KATP channel). In cells preincubated for 30 min in a solution containing CoQ10 (100 micrograms/ml), CN(-)-activation of the KATP channel was markedly attenuated both at the whole cell and at the single channel level. At the steady-state effect of CN- in CoQ10-treated cells, pinacidil (300 microM) activated the current to the maximum level achieved by CN- in the control cells. These results suggest that CoQ10 reduces in the CN(-)-induced KATP current not by affecting the channel itself but by preventing depletion of intracellular ATP caused by CN-.
采用膜片钳技术,在单个心房肌细胞中研究了辅酶Q10(CoQ10)对氰化物(CN-)诱导的ATP敏感性钾通道电流(KATP)的影响。用CN-/低糖灌流液灌流细胞,在全细胞钳制条件下诱导出外向电流。格列本脲(1 microM)可消除该电流,表明该电流是通过KATP通道传导的。在经CN-稳态激活后,吡那地尔(一种KATP通道开放剂,300 microM)未能进一步增加电流。在细胞贴附膜片上,将CN-施加于灌流液时,可诱导一个80 pS通道(KATP通道)出现爆发性开放。在含有CoQ10(100微克/毫升)的溶液中预孵育30分钟的细胞中,无论是在全细胞水平还是单通道水平,CN-对KATP通道的激活均明显减弱。在CoQ10处理的细胞中,在CN-的稳态作用下,吡那地尔(300 microM)可将电流激活至对照细胞中CN-所达到的最大水平。这些结果表明,CoQ10降低CN-诱导的KATP电流,不是通过影响通道本身,而是通过防止CN-引起的细胞内ATP耗竭来实现的。