Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, 01601, Ukraine.
Biochemistry (Mosc). 2010 Sep;75(9):1139-47. doi: 10.1134/s0006297910090075.
The influence of the K+(ATP)-channel opener diazoxide on the K+ cycle and oxygen consumption has been studied in rat liver mitochondria. It was found that diazoxide activates the K+(ATP)-channel in the range of nanomolar concentrations (50-300 nM, K(1/2) ~ 140 nM), which results in activation of K+/H+ exchange in mitochondria. The latter, in turn, accelerates mitochondrial respiration in respiratory state 2. The contribution of K+(ATP)-channel to the mitochondrial potassium cycle was estimated using the selective K+(ATP)-channel blocker glibenclamide. The data show that the relative contribution of K+(ATP)-channel in the potassium cycle of mitochondria is variable and increases only with the decrease in the ATP-independent component of K+ uptake. Possible mechanisms underlying the observed phenomena are discussed. The experimental results more fully elucidate the role of K+(ATP)-channel in the regulation of mitochondrial functions, especially under pathological conditions accompanied by impairment of the mitochondrial energy state.
已在大鼠肝线粒体中研究了 K+(ATP)-通道 opener 二氮嗪对 K+循环和耗氧量的影响。结果发现,二氮嗪在纳摩尔浓度范围内(50-300 nM,K(1/2)~140 nM)激活 K+(ATP)-通道,这导致线粒体中 K+/H+交换的激活。反过来,这又加速了呼吸状态 2 中的线粒体呼吸。使用选择性 K+(ATP)-通道阻断剂 glibenclamide 估计 K+(ATP)-通道对线粒体钾循环的贡献。数据表明,K+(ATP)-通道在线粒体钾循环中的相对贡献是可变的,并且仅在 K+摄取的 ATP 非依赖性成分减少时才增加。讨论了观察到的现象的可能机制。实验结果更充分地阐明了 K+(ATP)-通道在调节线粒体功能中的作用,特别是在伴有线粒体能量状态受损的病理条件下。