Nitroglycerin-Induced Endothelial Dysfunction and Tolerance Involve Adverse Phosphorylation and S -Glutathionylation of Endothelial Nitric Oxide Synthase: Beneficial Effects of Therapy With the AT 1 Receptor Blocker Telmisartan
Abstract
Objective—: Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT 1 )-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S -glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP–cyclohydrolase I. Methods and Results—: Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phosphorylation and S -glutathionylation were assessed using antibodies against phospho-Thr495 and Ser1177 or protein-bound glutathione, which regulate eNOS activity and eNOS-dependent superoxide production (uncoupling). Expression of mitochondrial aldehyde dehydrogenase was determined by Western blotting. Formation of aortic and cardiac ROS was assessed by fluorescence, chemiluminescence, and 3-nitrotyrosine/malondialdehyde-positive protein content. Telmisartan prevented endothelial dysfunction and partially improved nitrate tolerance. Vascular, cardiac, mitochondrial, and white blood cell ROS formation were significantly increased by GTN treatment and inhibited by telmisartan. GTN-induced decrease in Ser1177, increase in Thr495 phosphorylation or S -glutathionylation of eNOS, and decrease in mitochondrial aldehyde dehydrogenase expression were normalized by telmisartan. Conclusion—: These data identify modification of eNOS phosphorylation as an important component of GTN-induced endothelial dysfunction. Via its pleiotropic “antioxidant” properties, telmisartan prevents, at least in part, GTN-induced oxidative stress, nitrate tolerance, and endothelial dysfunction.
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S-glutathionylation increases eNOS uncoupling and formation of superoxide with diminished NO synthesis activity.
“The reaction increases eNOS uncoupling and the formation of superoxide with diminished NO synthesis activity.”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [522]
S-glutathionylation is involved in angiotensin II-mediated endothelial dysfunction and nitroglycerin resistance.
“S-glutathionylation has been involved in the development of angiotensin II–mediated endothelial dysfunction (328) and nitroglycerin resistance (522).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [522]
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- Authors
- Knorr, M., Hausding, M., Kröller-Schuhmacher, S., Steven, S., Oelze, M., Heeren, T., Scholz, A., Gori, T., Wenzel, P., Schulz, E., Daiber, A., & Münzel, T.
- Affiliations
- Johannes Gutenberg University Mainz (DE)
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2011-10
- Volume
- 31
- Issue
- 10
- Pages
- 2223-2231
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2118676803
- Cited by
- 100
- References
- 39
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 8 · 2019: 5 · 2018: 9 · 2017: 11 · 2016: 6 · 2015: 9 · 2014: 12 · 2013: 15 · 2012: 10
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- nitroglycerin, endothelial dysfunction, nitrate tolerance, endothelial nitric oxide synthase, eNOS phosphorylation, S-glutathionylation, telmisartan, angiotensin II type 1 receptor blockade, reactive oxygen species, oxidative stress, eNOS uncoupling, mitochondrial aldehyde dehydrogenase, GTP cyclohydrolase I, superoxide production, nitrotyrosine, malondialdehyde
- MeSH terms
- Telmisartan, Aldehyde Dehydrogenase, Animals, Benzimidazoles, Benzoates, Cell Line, Dose-Response Relationship, Drug, Drug Tolerance, Endothelium, Vascular, Enzyme Inhibitors, Glutathione, Nitroglycerin, GTP Cyclohydrolase, Humans, Male, Mitochondria, Phosphorylation, Protein Processing, Post-Translational, Tetrahydrofolate Dehydrogenase, Vasodilation, Vasodilator Agents, Rats, Wistar, Reactive Oxygen Species, Oxidative Stress, Endothelial Cells, Angiotensin II Type 1 Receptor Blockers, Rats, Nitric Oxide Synthase Type III
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