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.

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