Cited by 300Nitric Oxide and Endothelin EffectsMitochondrial Function and PathologyEicosanoids and Hypertension Pharmacology

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Central role of mitochondrial aldehyde dehydrogenase and reactive oxygen species in nitroglycerin tolerance and cross-tolerance

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Sydow, Karsten, Daiber, Andreas, Oelze, Matthias, Chen, Zhiqiang, August, Michael, Wendt, Maria, Ullrich, Volker, Mülsch, Alexander, Schulz, Eberhard, Keaney, John F., Stamler, Jonathan S., Münzel, Thomas·2004·Journal of Clinical Investigation

DOI 10.1172/jci200419267

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Abstract

Recent studies suggest that mitochondrial aldehyde dehydrogenase (ALDH-2) plays a central role in the process of nitroglycerin (glyceryl trinitrate, GTN) biotransformation in vivo and that its inhibition accounts for mechanism-based tolerance in vitro. The extent to which ALDH-2 contributes to GTN tolerance (impaired relaxation to GTN) and cross-tolerance (impaired endothelium-dependent relaxation) in vivo remain to be elucidated. Rats were treated for three days with GTN. Infusions were accompanied by decreases in vascular ALDH-2 activity, GTN biotransformation, and cGMP-dependent kinase (cGK-I) activity. Further, whereas in control vessels, multiple inhibitors and substrates of ALDH-2 reduced both GTN-stimulation of cGKI and GTN-induced vasodilation, these agents had little effect on tolerant vessels. A state of functional tolerance (in the GTN/cGMP pathway) was recapitulated in cultured endothelial cells by knocking down mitochondrial DNA (ρ0 cells). In addition, GTN increased the production of reactive oxygen species (ROS) by mitochondria, and these increases were associated with impaired relaxation to acetylcholine. Finally, antioxidants/reductants decreased mitochondrial ROS production and restored ALDH-2 activity. These observations suggest that nitrate tolerance is mediated, at least in significant part, by inhibition of vascular ALDH-2 and that mitochondrial ROS contribute to this inhibition. Thus, GTN tolerance may be viewed as a metabolic syndrome characterized by mitochondrial dysfunction.

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Authors: Sydow, K., Daiber, A., Oelze, M., Chen, Z., August, M., Wendt, M., Ullrich, V., Mülsch, A., Schulz, E., Keaney, J. F., Stamler, J. S., & Münzel, T.
Affiliations: University Medical Center Hamburg-Eppendorf (DE)
Howard Hughes Medical Institute (US)
University of Konstanz (DE)
Goethe University Frankfurt (DE)
Boston University (US)
Corresponding author: Münzel, Thomas
ORCID: Daiber, Andreas
Oelze, Matthias
Chen, Zhiqiang
Wendt, Maria
Schulz, Eberhard
Keaney, John F.
Stamler, Jonathan S.
Münzel, Thomas
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2004-02-01
Volume: 113
Issue: 3
Pages: 482-489
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci200419267
OpenAlex: W2172008520
Cited by: 300
References: 38
Citations by year: 2025: 5 · 2024: 3 · 2023: 6 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 10 · 2017: 17 · 2016: 11 · 2015: 11 · 2014: 12 · 2013: 7 · 2012: 18
FWCI: 18.50
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords: nitroglycerin tolerance, nitrate tolerance, mitochondrial aldehyde dehydrogenase, reactive oxygen species, endothelium-dependent relaxation, mitochondrial dysfunction, antioxidants, acetylcholine-induced relaxation, vascular smooth muscle
MeSH terms: Aldehyde Dehydrogenase, Animals, Aorta, Drug Tolerance, Nitroglycerin, Cyclic GMP, Mitochondria, Myocardium, Vasodilator Agents, Rats, Wistar, Reactive Oxygen Species, Models, Animal, Rats

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Central role of mitochondrial aldehyde dehydrogenase and reactive oxygen species in nitroglycerin tolerance and cross-tolerance

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