ArticleBritish journal of pharmacology2011
Decreased production of neuronal NOS-derived hydrogen peroxide contributes to endothelial dysfunction in atherosclerosis.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 64 citations in OpenAlex.
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- Natural flavonoids derived from herbal medicines are potential anti-atherogenic agents by inhibiting oxidative stress in endothelial cells.Frontiers in pharmacology · 2023Review
- Targeting Reactive Oxygen Species in Atherosclerosis via Chinese Herbal Medicines.Oxidative medicine and cellular longevity · 2022Review
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- Amitriptyline Downregulates Chronic Inflammatory Response to Biomaterial in Mice.Inflammation · 2021Article
- SIRT1-induced deacetylation of Akt expedites platelet phagocytosis and delays HEMEC aging.Molecular therapy. Nucleic acids · 2021Article
- Role of neuronal nitric oxide synthase on cardiovascular functions in physiological and pathophysiological states.Nitric oxide : biology and chemistry · 2020Review
- Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS?International journal of molecular sciences · 2019Review
- New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis.Redox biology · 2019Review
- Protective Role of Perivascular Adipose Tissue in Endothelial Dysfunction and Insulin-Induced Vasodilatation of Hypercholesterolemic LDL Receptor-Deficient Mice.Frontiers in physiology · 2018Article
- The human coronary vasodilatory response to acute mental stress is mediated by neuronal nitric oxide synthase.American journal of physiology. Heart and circulatory physiology · 2017Article
- Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress.F1000Research · 2017Review
- Vascular Kinin BFrontiers in physiology · 2017Article
- Nitric Oxide and Hydrogen Sulfide Interact When Modulating Gastric Physiological Functions in Rodents.Digestive diseases and sciences · 2017Article
- Aerobic exercise training protects against endothelial dysfunction by increasing nitric oxide and hydrogen peroxide production in LDL receptor-deficient mice.Journal of translational medicine · 2016Article
- Significant Modules and Biological Processes between Active Components of Salvia miltiorrhiza Depside Salt and Aspirin.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- Neuronal Nitric Oxide Synthase in Vascular Physiology and Diseases.Frontiers in physiology · 2016Review
- Vascular dysfunctions in the isolated aorta of double-transgenic hypertensive mice developing aortic aneurysm.Pflugers Archiv : European journal of physiology · 2015Article
- Acid-sensing ion channel 1 and nitric oxide synthase are in adjacent layers in the wall of rat and human cerebral arteries.Journal of chemical neuroanatomy · 2014Article
- Paraquat poisoning induces TNF-α-dependent iNOS/NO mediated hyporesponsiveness of the aorta to vasoconstrictors in rats.PloS one · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeReduced NO availability has been described as a key mechanism responsible for endothelial dysfunction in atherosclerosis. We previously reported that neuronal NOS (nNOS)-derived H(2)O(2) is an important endothelium-derived relaxant factor in the mouse aorta. The role of H(2)O(2) and nNOS in endothelial dysfunction in atherosclerosis remains undetermined. We hypothesized that a decrease in nNOS-derived H(2)O(2) contributes to the impaired vasodilatation in apolipoprotein E-deficient mice (ApoE(-/-)). EXPERIMENTAL APPROACH: Changes in isometric tension were recorded on a myograph; simultaneously, NO and H(2)O(2) were measured using carbon microsensors. Antisense oligodeoxynucleotides were used to knockdown eNOS and nNOS in vivo. Western blot and confocal microscopy were used to analyse the expression and localization of NOS isoforms. KEY
resultsAortas from ApoE(-/-) mice showed impaired vasodilatation paralleled by decreased NO and H(2)O(2) production. Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice. Confocal microscopy showed increased nNOS immunostaining in endothelial cells of ApoE(-/-) mice. However, ACh stimulation of vessels resulted in less phosphorylation on Ser852 in ApoE(-/-) mice. CONCLUSIONS AND IMPLICATIONS: Our data show that endothelial nNOS-derived H(2)O(2) production is impaired and contributes to endothelial dysfunction in ApoE(-/-) aorta. The present study provides a new mechanism for endothelial dysfunction in atherosclerosis and may represent a novel target to elaborate the therapeutic strategy for vascular atherosclerosis.
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