The mechanism of tissue protection from ischemic damage by activation of the mitochondrial
ATP-dependent K(+) channel (
mitoK(ATP)) remains unexplored. In this work, we have measured, using various approaches, the
ATP-dependent mitochondrial K(+) transport in rats that differed in their resistance to
hypoxia. The transport was found to be faster in the
hypoxia-resistant rats as compared to that in the
hypoxia-sensitive animals. Adaptation of animals to the intermittent normobaric
hypoxia increased the rate of transport. At the same time, the intramitochondrial concentration of K(+) in the
hypoxia-sensitive rats was higher than that in the resistant and adapted animals. This indicates that adaptation to
hypoxia stimulates not only the influx of
potassium into mitochondria, but also K(+)/H(+) exchange. When
mitoK(ATP) was blocked, the rate of the mitochondrial H(2)O(2) production was found to be significantly higher in the
hypoxia-resistant rats than that in the
hypoxia-sensitive animals. The natural
flavonoid-containing adaptogen
Extralife, which has an evident antihypoxic effect, increased the rate of the mitochondrial
ATP-dependent K(+) transport in vitro and increased the in vivo tolerance of
hypoxia-sensitive rats to acute
hypoxia 5-fold. The involvement of the mitochondrial K(+) transport in the mechanism of cell adaptation to
hypoxia is discussed.