Determination of the rate of K+ movement through potassium channels in isolated rat heart and liver mitochondria
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Both ATP-regulated (mitoK(ATP)) and large conductance calcium-activated (mitoBK(Ca)) potassium channels have been proposed to regulate mitochondrial K(+) influx and matrix volume and to mediate cardiac ischaemic preconditioning (IP). However, the specificity of the pharmacological agents used in these studies and the mechanisms underlying their effects on IP remain controversial. Here we used increasing concentrations of K(+)-ionophore (valinomycin) to stimulate respiration by rat liver and heart mitochondria in the presence of the K(+)/H(+) exchanger nigericin. This allowed rates of valinomycin-induced K(+) influx to be determined whilst parallel measurements of light scattering (A(520)) and matrix volume ((3)H(2)O and [(14)C]-sucrose) enabled rates of K(+) influx to be correlated with increases in matrix volume. Light scattering readily detected an increase in K(+) influx of <5 nmol K(+) min(-1) per mg protein corresponding to <2% mitochondrial matrix volume increase. In agreement with earlier data no light-scattering changes were observed in response to any mitoK(ATP) channel openers or blockers. However, the mitoBK(Ca) opener NS1619 (10-50 microM) did decrease light scattering slightly, but this was also seen in K(+)-free medium and was accompanied by uncoupling. Contrary to prediction, the mitoBK(Ca) blocker paxilline (10-50 microM) decreased rather than increased light scattering, and it also slightly uncoupled respiration. Our data argue against the presence of significant activities of either the mitoK(ATP) or the mitoBK(Ca) channel in rat liver and heart mitochondria and provide further evidence that preconditioning induced by pharmacological openers of these channels is more likely to involve alternative mechanisms.
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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 [27]
ROS trigger or mediate ischemic and pharmacologic preconditioning of hearts.
“It is now well known that ROS trigger or mediate ischemic and pharmacologic preconditioning of hearts (15, 27, 102, 181, 183, 248, 254, 303).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [27]
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Lai, Y.-R. (2013) · Elsevier eBooks · doi:10.1533/9781908818287.455 · Cited by 6 · see citing works
Potassium channel openers prevent palmitate-induced insulin resistance in C2C12 myotubes
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Khodaee, N., Ghasemi, M., Javad, F.-B., Saghiri, R., & Eliassi, A. (2014)
Evidences for a new cation channel in the brain mitochondrial inner membrane
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- Authors
- Bednarczyk, P., Barker, G. D., & Halestrap, A. P.
- Affiliations
- Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
- University of Bristol (GB)
- Corresponding author
- Halestrap, Andrew P.
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2008-06
- Volume
- 1777
- Issue
- 6
- Pages
- 540-548
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W1990179610
- Cited by
- 54
- References
- 55
- Citations by year
- 2024: 1 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 3 · 2014: 3 · 2013: 10 · 2012: 5
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Funders
- Novartis Foundation
- British Heart Foundation (RG/03/002/15663, RG/03/002)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- mitochondrial potassium channels, potassium influx, valinomycin, nigericin, NS1619, paxilline, uncoupled respiration, rat heart mitochondria, rat liver mitochondria
- MeSH terms
- Animals, Cations, Monovalent, Dose-Response Relationship, Drug, Ionophores, Male, Mitochondria, Heart, Mitochondria, Liver, Nigericin, Oxygen Consumption, Potassium, Valinomycin, Potassium Channels, Ion Transport, Rats, Wistar, Ischemic Preconditioning, Myocardial, Mitochondrial Proteins, Large-Conductance Calcium-Activated Potassium Channel alpha Subunits, Rats
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