Under the presence of succinate, the increase of O2 uptake with simultaneous decrease of ADP/O ratio in rats with high resistance under stress was observed. Simultaneously, oxidation of б-ketoglutarate, a NAD-dependent substrate, was inhibited. Pinacidil caused reorganization of mitochondrial energy metabolism in favor of NAD-dependent oxidation and improvement of the protection against stress. The decrease of the efficacy of mitochondrial energy processes functioning was shown in animals with low resistant to hypoxia. КATP channel opener pinacidil has a protective effect on the processes of mitochondrial liver energy support under stress. These changes deal with the increase of б-ketoglutarate oxidation (respiratory rate and ADP/O) and the decrease of lipid peroxidation processes. We concluded about protective effect of pinacidil on mitochondrial functioning under stress.
The adaptation by intermittent hypoxia and application of a KATP channel opener pinacidil possess significant protective effect on mitochondrial energy support under stress condition. Combination of intermittent hypoxia with pinacidil causes more efficient consumption of oxygen and decrease of lipid peroxidation processes comparative to intermittent hypoxia or pinacidil injection used separately. We conclude about the existence of the functional link between nitric oxide which is being increased under intermittent hypoxia and KATP channel opener. Both intermittent hypoxia and pinacidil effectively decrease the negative results of mitochondrial dysfunction under stress condition.
Key words: KATP-channels, pinacidil, glibenclamide, mitochondria, succinate, б-ketoglutarate, stress, myocardium dystrophy, intermittent hypoxia, ADP-stimulated respiration, lipid peroxidation processes.