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Opening of mitochondrial K(ATP) channels attenuates the ouabain-induced calcium overload in mitochondria

H Ishida1, Y Hirota, C Genka

  • 1Department of Physiology, Tokai University School of Medicine, Isehara, Japan.

Circulation Research
|November 10, 2001
PubMed

Insights

Opening mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channels prevents mitochondrial calcium overload by depolarizing the mitochondrial membrane potential. This mechanism protects the myocardium from ischemic damage.

Area of Science:

  • Cardiology
  • Mitochondrial Physiology
  • Cellular Electrophysiology

Background:

  • Mitochondrial calcium overload contributes to myocardial damage during ischemia.
  • Mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels are potential therapeutic targets.

Purpose of the Study:

  • To investigate if opening mitoK(ATP) channels prevents mitochondrial calcium overload by altering mitochondrial membrane potential.
  • To determine the protective role of mitoK(ATP) channel activation against ischemic damage.

Main Methods:

  • Rat ventricular myocytes were used to measure mitochondrial calcium concentration ([Ca(2+)](m)) and mitochondrial membrane potential (DeltaPsi(m)).
  • Confocal microscopy with Rhod-2 and JC-1 dyes was employed for real-time measurements.
  • Ouabain was used to induce mitochondrial calcium overload, and diazoxide was used to open mitoK(ATP) channels.

Main Results:

  • Ouabain significantly increased [Ca(2+)](m) (173% of baseline).
  • Diazoxide treatment attenuated ouabain-induced [Ca(2+)](m) overload (131% of baseline).
  • Diazoxide caused DeltaPsi(m) depolarization (89% of baseline) and this effect was blocked by 5-hydroxydecanoate.

Conclusions:

  • Opening mitoK(ATP) channels prevents mitochondrial calcium overload.
  • DeltaPsi(m) depolarization is associated with the protective effect of mitoK(ATP) channel opening.
  • Activation of mitoK(ATP) channels offers cardioprotection against ischemic damage.

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