Opening mitochondrial K ATP in the heart - what happens, and what does not happen
Abstract
There is considerable evidence that opening the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) is cardioprotective in ischemia-reperfusion. Two prominent questions surround the role of mitoK(ATP) in the cardiomyocyte: How does opening mitoK(ATP) protect? What is the normal physiological role of mitoK(ATP) in the heart? Before these questions can be addressed, it is necessary to agree on the bioenergetic consequences of opening mitoK(ATP), and this distills down to a single question--does opening mitoK(ATP) cause significant uncoupling or not? The evidence strongly indicates that it does not and that reports of uncoupling and inhibition of Ca2+ uptake are the result of using toxic concentrations of K(ATP) channel openers. Thus, opening mitoK(ATP) results in increased K+ flux that is sufficient to change mitochondrial volume but is insufficient to cause significant depolarization of membrane potential. The volume changes, however, have significant bioenergetic consequences for energy coupling in the cell.
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The mitochondrion likely releases small amounts of H2O2 as a natural chemical messenger in the modulation of mitochondrial and cellular function.
“Although the mitochondrion is largely a sink for O2•− and H2O2 due to its ROS scavenger systems, it likely releases small amounts of H2O2 as a natural chemical messenger in the modulation of mitochondrial and cellular function (27, 113, 126, 183, 203, 206).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [126]
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References 28 · Cited by 186
- Authors
- Garlid, K. D.
- Corresponding author
- Garlid, Keith D.
- ORCID
- Garlid, Keith D.
- Venue
- Basic Research in Cardiology
- Published
- 2000-08-01
- Volume
- 95
- Issue
- 4
- Pages
- 275-279
- ISSN
- 0003-9217 (ISSN-L)
- 0300-8428
- 1435-1803
- OpenAlex
- W2046712654
- Cited by
- 186
- References
- 28
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 10 · 2015: 4 · 2014: 6 · 2013: 3 · 2012: 5
- FWCI
- 10.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Basic Research in Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01gm055324-04)
- National Institute of General Medical Sciences (GM55324)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Keywords
- mitochondrial ATP-sensitive potassium channel, cardioprotection, ischemia-reperfusion injury, mitochondrial uncoupling, mitochondrial bioenergetics, potassium flux, mitochondrial volume, mitochondrial membrane potential, calcium uptake inhibition, KATP channel openers, cardiomyocytes
- MeSH terms
- Adenosine Triphosphate, Animals, Humans, Mitochondria, Heart, Potassium Channels, Ischemic Preconditioning
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