Akopova O V, Nosar' V I, Kolchinskaia L I, Man'kovskaia I N, Malysheva M K, Sagach V F
Ukr Biokhim Zh (1999). 2013 Jan-Feb;85(1):33-41.
The effect of potential-dependent potassium uptake on the transmembrane potential difference (DeltaPsi(m)) in rat brain mitochondria has been studied. It was shown that in potassium concentration range of 0-120 mM the potential-dependent K(+)-uptake into matrix leads to the increase in respiration rate and mitochondrial depolarization. ATP-dependent potassium channel (K+(ATP)-channel) blockers, glibenclamide and 5-hydroxydecanoate, block approximately 35% of potential-dependent potassium uptake in the brain mitochondria. It was shown that K+(ATP)-channel blockage results in membrane repolarization by approximately 20% of control, which is consistent with experimental dependence of DeltaPsi(m) on the rate of potential-dependent potassium uptake. Obtained experimental data give the evidence that functional activity of K+(ATP)-channel is physiologically important in the regulation of membrane potential and energy-dependent processes in brain mitochondria.
研究了电位依赖性钾摄取对大鼠脑线粒体跨膜电位差（ΔΨm）的影响。结果表明，在0 - 120 mM的钾浓度范围内，电位依赖性K⁺摄取进入基质会导致呼吸速率增加和线粒体去极化。ATP依赖性钾通道（K⁺(ATP)通道）阻滞剂格列本脲和5-羟基癸酸可阻断脑线粒体中约35%的电位依赖性钾摄取。结果表明，K⁺(ATP)通道阻滞导致膜复极化约为对照的20%，这与ΔΨm对电位依赖性钾摄取速率的实验依赖性一致。获得的实验数据证明，K⁺(ATP)通道的功能活性在调节脑线粒体膜电位和能量依赖性过程中具有重要的生理意义。
