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Inner Mitochondrial Membrane Sensitivity to Na+ Reveals Partially Segmented Functional CoQ Pools
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A novel mitochondrial K(ATP) channel assay.

Andrew P Wojtovich1, David M Williams, Marcin K Karcz

  • 1Department of Pharmacology, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA.

Circulation Research
|February 27, 2010
PubMed
Summary

Researchers developed a new thallium flux assay to measure mitochondrial ATP-sensitive potassium channel (mK(ATP)) activity. This assay revealed fluoxetine inhibits mK(ATP) and blocks preconditioning-induced cardioprotection.

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Area of Science:

  • Cardiovascular Research
  • Mitochondrial Physiology
  • Ion Channel Pharmacology

Background:

  • The mitochondrial ATP-sensitive potassium channel (mK(ATP)) plays a role in cardioprotection during ischemic preconditioning (IPC).
  • The precise molecular identity and reliable assay methods for mK(ATP) remain subjects of debate.
  • Current techniques for assessing mK(ATP) activity are disputed, hindering research progress.

Purpose of the Study:

  • To develop and validate novel methodologies for assaying mitochondrial ATP-sensitive potassium channel (mK(ATP)) activity.
  • To investigate the regulation of mK(ATP) by key signaling molecules and pharmacological agents.
  • To explore the role of mK(ATP) in ischemic preconditioning-induced cardioprotection.

Main Methods:

  • Development of a novel thallium (Tl(+)) flux-based assay utilizing a Tl(+)-sensitive fluorophore to measure mK(ATP) activity.
  • Application of the Tl(+) flux assay to investigate the effects of phosphatidylinositol-4,5-bisphosphate (PIP(2)), nucleotides (ATP, UDP), and the antidepressant fluoxetine on mK(ATP) function.
  • Validation of the Tl(+) flux assay by correlating its results with a classical osmotic swelling assay for mK(ATP).

Main Results:

  • The novel thallium (Tl(+)) flux assay successfully measured mK(ATP) activity.
  • mK(ATP) activity was modulated by phosphatidylinositol-4,5-bisphosphate (PIP(2)) and nucleotides, with specific EC(50) and IC(50) values determined for UDP and ATP.
  • The antidepressant fluoxetine significantly inhibited mK(ATP) activity (IC(50)=2.4 micromol/L) and blocked ischemic preconditioning (IPC)-induced cardioprotection, while zimelidine had no effect.

Conclusions:

  • The thallium (Tl(+)) flux assay is a validated and reliable method for assessing mK(ATP) activity, correlating well with established assays.
  • The pharmacological profile of mK(ATP) suggests it functions as an inward rectifying potassium channel (K(IR)), potentially the K(IR)6.2 isoform.
  • The inhibition of mK(ATP)-dependent cardioprotection by fluoxetine highlights potential implications for antidepressant use in patients susceptible to ischemic events.