ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel

Lebuffe, Gilles; Schumacker, Paul T.; Shao, Zuo-Hui; Anderson, Travis; Iwase, Hirotoro; Vanden Hoek, Terry L.

doi:10.1152/ajpheart.00706.2002

Cited by 227Cardiac Ischemia and ReperfusionCell death mechanisms and regulationNitric Oxide and Endothelin Effects

ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel

Lebuffe, Gilles, Schumacker, Paul T., Shao, Zuo-Hui, Anderson, Travis, Iwase, Hirotoro, Vanden Hoek, Terry L.·2003·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00706.2002

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Abstract

Reactive oxygen species (ROS) and nitric oxide (NO) are implicated in induction of ischemic preconditioning. However, the relationship between these oxidant signals and opening of the mitochondrial ATP-dependent potassium (K ATP) channel during early preconditioning is not fully understood. We observed preconditioning protection by hypoxia, exogenous H 2 O 2, or PKC activator PMA in cardiomyocytes subjected to 1-h ischemia and 3-h reperfusion. Protection was abolished by K ATP channel blocker 5-hydroxydecanoate (5-HD) in each case, indicating that these triggers must act upstream from the K ATP channel. Inhibitors of NO synthase abolished protection in preconditioned cells, suggesting that NO is also required for protection. DAF-2 fluorescence (NO sensitive) increased during hypoxic triggering. This was amplified by pinacidil and inhibited by 5-HD, indicating that NO is generated subsequent to K ATP channel activation. Exogenous NO during the triggering phase conferred protection blocked by 5-HD. Exogenous NO also restored protection abolished by 5-HD or N ω-nitro-l-arginine methyl ester in preconditioned cells. Antioxidants given during pinacidil or NO triggering abolished protection, confirming that ROS are generated by K ATP channel activation. Coadministration of H 2 O 2 and NO restored PMA-induced protection in 5-HD-treated cells, indicating that ROS and NO are required downstream from the K ATP channel. We conclude that ROS can trigger preconditioning by causing activation of the K ATP channel, which then induces generation of ROS and NO that are both required for preconditioning protection.

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Once in a high redox state, QH• can lose its unpaired electron to O2 as all upstream redox centers are fully reduced.
“Once in a high redox state, QH• can lose its unpaired electron to O2 as all upstream redox centers are fully reduced (200).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [200]

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Authors: Lebuffe, G., Schumacker, P. T., Shao, Z.-H., Anderson, T., Iwase, H., & Vanden Hoek, T. L.
Affiliations: University of Chicago (US)
Department of Medicine, Emergency Resuscitation Center, University of Chicago, Chicago, Illinois 60637
ORCID: Lebuffe, Gilles
Schumacker, Paul T.
Anderson, Travis
Venue: American Journal of Physiology-Heart and Circulatory Physiology
Publisher: American Physiological Society
Published: 2003-01-01
Volume: 284
Issue: 1
Pages: H299-H308
ISSN: 0363-6135 (ISSN-L)
1522-1539
DOI: 10.1152/ajpheart.00706.2002
OpenAlex: W2130229822
Cited by: 227
References: 54
Citations by year: 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 9 · 2016: 4 · 2015: 6 · 2014: 8 · 2013: 7 · 2012: 10
FWCI: 15.08
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords: ischemic preconditioning, reactive oxygen species, nitric oxide, mitochondrial ATP-dependent potassium channel, ATP-sensitive potassium channels, cardiomyocytes, hypoxia, hydrogen peroxide, protein kinase C, 5-hydroxydecanoate, nitric oxide synthase, antioxidants, myocardial ischemia-reperfusion injury, cardioprotection
MeSH terms: Adenosine Triphosphate, Animals, Cells, Cultured, Chick Embryo, Hydrogen Peroxide, Mitochondria, Heart, Nitric Oxide, Protein Kinase C, Potassium Channels, Oxidants, Reactive Oxygen Species, Ischemic Preconditioning, Myocardial, Myocytes, Cardiac

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ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel

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