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Mitochondrial ATP-sensitive K+ channels modulate cardiac mitochondrial function

E L Holmuhamedov1, S Jovanović, P P Dzeja

  • 1Division of Cardiovascular Diseases, Department of Medicine and Pharmacology, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA.

The American Journal of Physiology
|November 14, 1998
PubMed
Summary
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Activation of ATP-sensitive potassium (KATP) channels in cardiac mitochondria depolarizes the membrane, increases respiration, and affects calcium transport. This research clarifies the role of mitochondrial KATP channels in heart function.

Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Ion Channel Function

Background:

  • ATP-sensitive potassium (KATP) channels are found in cardiac sarcolemma and inner mitochondrial membranes.
  • The precise impact of mitochondrial KATP channel activation on cardiac mitochondrial function requires further elucidation.

Purpose of the Study:

  • To investigate the functional consequences of activating mitochondrial KATP channels in isolated rat cardiac mitochondria.
  • To assess the effects on mitochondrial membrane potential, respiration, ATP synthesis, calcium handling, and matrix volume.

Main Methods:

  • Isolated rat cardiac mitochondria were treated with KATP channel openers (pinacidil, cromakalim, levcromakalim).
  • Measurements included mitochondrial membrane potential, respiration rates, ATP production, Ca2+ transport, and matrix volume.

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  • Effects were assessed with and without extramitochondrial K+ and in the presence of KATP channel blockers.

    • Main Results:

    • KATP channel openers induced significant mitochondrial membrane depolarization.
    • Depolarization correlated with increased mitochondrial respiration and decreased ATP synthesis.
    • Activation led to Ca2+ release from mitochondria, mitochondrial swelling, and release of intermembrane proteins like cytochrome c.

    Conclusions:

    • Mitochondrial KATP channel activation in cardiac mitochondria causes membrane depolarization, altered energy metabolism, and release of matrix and intermembrane proteins.
    • These findings highlight a critical role for mitochondrial KATP channels in regulating cardiac mitochondrial function and cellular integrity.