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

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

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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Crossref · 10.1152/ajpheart.00706.2002

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Metadata

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
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 › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Physiology (medical) › 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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