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Cited by 304

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Endothelial Function and Oxidant Stress

Open access
Harrison, David G.·1997·Clinical Cardiology
DOI 10.1002/j.1932-8737.1997.tb00007.x
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Abstract

Both endothelial cells and vascular smooth muscle cells are capable of producing reactive oxygen species from a variety of enzymatic sources. In disease states such as atherosclerosis and hypertension, vascular production of these reactive oxygen metabolites can increase substantially. Increases in the production of superoxide anion can lead to decreases in ambient levels of nitric oxide via a facile radical/radical reaction that occurs more rapidly than the reaction of superoxide anion with superoxide dismutase. This phenomenon alters endothelial regulation of vasomotion in a variety of disease conditions. Recent evidence suggests that the major source of vascular superoxide ion and hydrogen peroxide is a membrane‐bound, reduced nicotinamide‐adenine dinucleotide (NADH)‐dependent oxidase. The activity of this enzyme system is regulated by angiotensin II and is elevated following prolonged exposure to nitroglycerin. Alterations of vascular oxidant state caused by angiotensin II may contribute substantially to vascular pathology and may also provide a link between hypertension and atherosclerosis.

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Crossref · 10.1002/j.1932-8737.1997.tb00007.x

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Citations

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Cited by

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Metadata

Authors
Harrison, D. G.
Venue
Clinical Cardiology
Publisher
Wiley
Published
1997-10
Volume
20
Issue
S2
Pages
II-11
ISSN
  • 0160-9289 (ISSN-L)
  • 1932-8737
DOI
10.1002/j.1932-8737.1997.tb00007.x
OpenAlex
W156498367
Cited by
304
References
7
FWCI
4.78
Type
journal article
Language
en
Open access
bronze

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Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.