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Cited by 342

The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.

Reactive oxygen species in hypertension*1An update

LASSEGUE, B·2004·American Journal of Hypertension
DOI 10.1016/j.amjhyper.2004.02.004
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Abstract

Hypertension is associated with an elevation of reactive oxygen species (ROS) and frequently also with an impairment of endogenous antioxidant mechanisms. Experimental manipulation of the redox state in vivo shows that ROS can be a cause of hypertension. During the development of the disease, ROS are generated by endogenous sources, notably the NADPH oxidase enzyme family and uncoupled nitric oxide synthase, due to a mutual reinforcement between ROS and humoral factors. The ROS affect multiple tissues, either directly or through nitric oxide depletion. In the vasculature, they induce contraction and endothelial dysfunction. In blood vessels and myocardium, they cause hypertrophic remodeling. In the kidneys, ROS promote salt reabsorption, decrease glomerular filtration, and lead to tissue damage. Finally, they also increase efferent sympathetic activity from the central nervous system. Progress in our understanding of the mechanisms of ROS formation and their plethora of pathophysiologic effects is expected to lead from simple antioxidant therapy to specific antihypertensive treatments.

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Metadata

Authors
LASSEGUE, B.
Venue
American Journal of Hypertension
Publisher
Oxford University Press (OUP)
Published
2004-09
Volume
17
Issue
9
Pages
852-860
ISSN
0895-7061 (ISSN-L)
DOI
10.1016/j.amjhyper.2004.02.004
OpenAlex
W2004301150
Cited by
342
References
71
FWCI
13.11
Type
journal article
Language
en
Open access
closed

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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.