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Structural and Dynamic Changes in Mitochondria of Rat Myocardium under Acute Hypoxic Hypoxia: Role of Mitochondrial ATP-Dependent Potassium Channel

E. V. Rozova1, I. N. Mankovskaya1, and G. D. Mironova2,3*

1Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, ul. Bogomoltsa 4, 01024 Kiev, Ukraine; E-mail: erozova@ukr.net

2Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, ul. Institutskaya 3, 142290 Pushchino, Moscow Region, Russia; E-mail: mironova40@mail.ru

3Pushchino State Institute of Natural Sciences, pr. Nauki 3, 142290 Pushchino, Moscow Region, Russia

* To whom correspondence should be addressed.

Received July 1, 2014; Revision received February 9, 2015
The ultrastructure and spatial localization of mitochondria (MC) in the myocardium of rats exposed to a 30-min hypoxic hypoxia were investigated. The mitochondrial structure was found to undergo changes; however, marked necrotic injuries were not observed. Changes occurring in the myocardium are aimed at the intensification of energy processes. This shows up as an increase in the number of MC in the subsarcolemmal zone of the myocardium and changes in the surface of the sublemmal membrane due to its bending around mitochondria, which improves the diffusion of oxygen into MC. In addition, the division of MC is enhanced, which partially explains the increase in their total number. In structurally altered MC with intact membrane, electron dense formations with small diameter appear, which probably represent newly formed organelles (microMC). In normoxia, changes of this kind do not occur. It was found that the ATP-dependent K+ channel is involved in the regulation of the morphological state of MC under hypoxic hypoxia. The activator of the channel diazoxide increases the number of newly formed microMC, and the channel inhibitor 5HD significantly prevents their formation. Possible mechanisms of structural and dynamic changes in rat myocardial MC under acute hypoxic hypoxia are discussed.
KEY WORDS: mitochondria, hypoxic hypoxia, ultrastructure, spatial localization, ATP-dependent K+ channel, channel modulators

DOI: 10.1134/S0006297915080040