Cited by 710Nitric Oxide and Endothelin EffectsMitochondrial Function and PathologyRenin-Angiotensin System Studies

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Molecular Mechanisms of Angiotensin II–Mediated Mitochondrial Dysfunction: Linking Mitochondrial Oxidative Damage and Vascular Endothelial Dysfunction

Doughan, Abdulrahman K., Harrison, David G., Dikalov, Sergey I.·2008·Circulation Research

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Abstract

Mitochondrial dysfunction is a prominent feature of most cardiovascular diseases. Angiotensin (Ang) II is an important stimulus for atherogenesis and hypertension; however, its effects on mitochondrial function remain unknown. We hypothesized that Ang II could induce mitochondrial oxidative damage that in turn might decrease endothelial nitric oxide (NO · ) bioavailability and promote vascular oxidative stress. The effect of Ang II on mitochondrial ROS, mitochondrial respiration, membrane potential, glutathione, and endothelial NO · was studied in isolated mitochondria and intact bovine aortic endothelial cells using electron spin resonance, dihydroethidium high-performance liquid chromatography –based assay, Amplex Red and cationic dye fluorescence. Ang II significantly increased mitochondrial H 2 O 2 production. This increase was blocked by preincubation of intact cells with apocynin (NADPH oxidase inhibitor), uric acid (scavenger of peroxynitrite), chelerythrine (protein kinase C inhibitor), N G -nitro- l -arginine methyl ester (nitric oxide synthase inhibitor), 5-hydroxydecanoate (mitochondrial ATP-sensitive potassium channels inhibitor), or glibenclamide. Depletion of p22 phox subunit of NADPH oxidase with small interfering RNA also inhibited Ang II–mediated mitochondrial ROS production. Ang II depleted mitochondrial glutathione, increased state 4 and decreased state 3 respirations, and diminished mitochondrial respiratory control ratio. These responses were attenuated by apocynin, 5-hydroxydecanoate, and glibenclamide. In addition, 5-hydroxydecanoate prevented the Ang II–induced decrease in endothelial NO · and mitochondrial membrane potential. Therefore, Ang II induces mitochondrial dysfunction via a protein kinase C–dependent pathway by activating the endothelial cell NADPH oxidase and formation of peroxynitrite. Furthermore, mitochondrial dysfunction in response to Ang II modulates endothelial NO · and generation, which in turn has ramifications for development of endothelial dysfunction.

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Self-citation
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Authors: Doughan, A. K., Harrison, D. G., & Dikalov, S. I.
Affiliations: United States Department of Veterans Affairs (US)
ORCID: Harrison, David G.
Dikalov, Sergey I.
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2008-02-29
Volume: 102
Issue: 4
Pages: 488-496
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/circresaha.107.162800
OpenAlex: W2164444293
Cited by: 710
References: 43
Citations by year: 2026: 24 · 2025: 24 · 2024: 19 · 2023: 32 · 2022: 33 · 2021: 44 · 2020: 39 · 2019: 31 · 2018: 31 · 2017: 36 · 2016: 54 · 2015: 29 · 2014: 58 · 2013: 51 · 2012: 50
FWCI: 25.60
Type: journal article
Language: en
Open access: closed
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
Funders: American Heart Association
National Institutes of Health (5p01hl075209-05)
National Heart, Lung, and Blood Institute (P0-1 HL-075209, R01HL094469, P01HL058000)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Keywords: angiotensin II, mitochondrial dysfunction, endothelial nitric oxide, NADPH oxidase, peroxynitrite, protein kinase C, mitochondrial reactive oxygen species, mitochondrial glutathione, mitochondrial respiration, endothelial dysfunction, oxidative stress, atherogenesis, hypertension
MeSH terms: Angiotensin II, Animals, Aorta, Cattle, Cells, Cultured, Glutathione, Hydrogen Peroxide, Mitochondria, Nitric Oxide, Superoxides, Vascular Diseases, Vasoconstrictor Agents, Oxidative Stress, Cell Respiration, Mitochondrial Diseases, Endothelial Cells, Membrane Potential, Mitochondrial

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Molecular Mechanisms of Angiotensin II–Mediated Mitochondrial Dysfunction: Linking Mitochondrial Oxidative Damage and Vascular Endothelial Dysfunction

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