KATP channel‐independent targets of diazoxide and 5‐hydroxydecanoate in the heart
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Diazoxide and 5‐hydroxydecanoate (5‐HD; C10:0) are reputed to target specifically mitochondrial ATP‐sensitive K+ (K ATP) channels. Here we describe K ATP channel‐independent targets of diazoxide and 5‐HD in the heart. Using submitochondrial particles isolated from pig heart, we found that diazoxide (10‐100 μ m) dose‐dependently decreased succinate oxidation without affecting NADH oxidation. Pinacidil, a non‐selective K ATP channel opener, did not inhibit succinate oxidation. However, it selectively inhibited NADH oxidation. These direct inhibitory effects of diazoxide and pinacidil cannot be explained by activation of mitochondrial K ATP channels. Furthermore, application of either diazoxide (100 μ m) or pinacidil (100 μ m) did not decrease mitochondrial membrane potential, assessed using TMRE (tetramethylrhodamine ethyl ester), in isolated guinea‐pig ventricular myocytes. We also tested whether 5‐HD, a medium‐chain fatty acid derivative which blocks diazoxide‐induced cardioprotection, was ‘activated’ via acyl‐CoA synthetase (EC 6.2.1.3), an enzyme present both on the outer mitochondrial membrane and in the matrix. Using analytical HPLC and electrospray ionisation mass spectrometry, we showed that 5‐HD‐CoA (5‐hydroxydecanoyl‐CoA) is indeed synthesized from 5‐HD and CoA via acyl‐CoA synthetase. Thus, 5‐HD‐CoA may be the active form of 5‐HD, serving as substrate for (or inhibiting) acyl‐CoA dehydrogenase (β‐oxidation) and/or exerting some other cellular action. In conclusion, we have identified K ATP channel‐independent targets of 5‐HD, diazoxide and pinacidil. Our findings question the assumption that sensitivity to diazoxide and 5‐HD implies involvement of mitochondrial K ATP channels. We propose that pharmacological preconditioning may be reelated to partial inhibition of respiratory chain complexes.
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Diazoxide inhibits complex II, while the KATP channel antagonist 5-HD can be metabolized by mitochondrial β-oxidation.
“Diazoxide inhibits complex II [128,129,147], while the K ATP channel antagonist 5-HD can be metabolized by the ß-oxidation pathway of the mitochondria [148][149][150].”
From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [128]
O2•− arises directly from the reduction of O2 by transfer of a lone electron to its antibonding orbital.
“O2•− arises directly from the reduction of O2 by transfer of a lone electron to its antibonding orbital (151).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [151]
The most direct and selective approach to measure specific ROS, notably in the matrix, is to use electron paramagnetic resonance (EPR).
“The most direct and selective approach to measure specific ROS, notably in the matrix, is to use electron paramagnetic resonance (EPR) (16, 129, 151).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [151]
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- Authors
- Hanley, P. J., Mickel, M., Löffler, M., Brandt, U., & Daut, J.
- Affiliations
- Philipps University of Marburg (DE)
- Goethe University Frankfurt (DE)
- Corresponding author
- Daut, Jürgen
- ORCID
- Brandt, Ulrich
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2002-08
- Volume
- 542
- Issue
- 3
- Pages
- 735-741
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC2290447
- OpenAlex
- W2013033853
- Cited by
- 320
- References
- 31
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 6 · 2016: 9 · 2015: 9 · 2014: 5 · 2013: 14 · 2012: 16
- FWCI
- 25.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- 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
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- diazoxide, 5-hydroxydecanoate, pinacidil, mitochondrial ATP-sensitive potassium channel, succinate oxidation, NADH oxidation, acyl-CoA synthetase, acyl-CoA dehydrogenase, fatty acid beta-oxidation, mitochondrial membrane potential, cardioprotection, pharmacological preconditioning, electron transport inhibition, heart mitochondria
- MeSH terms
- Long-Chain-Fatty-Acid-CoA Ligase, Acyl Coenzyme A, Adenosine Triphosphate, Animals, Coenzyme A Ligases, Decanoic Acids, Diazoxide, Electron Transport, Flavoproteins, Fluorescence, Guinea Pigs, Heart, Hydroxy Acids, Membrane Potentials, Mitochondria, Heart, Myocardium, Repressor Proteins, Potassium Channels, Pinacidil, Saccharomyces cerevisiae Proteins
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