| Heart failure, redox alterations, and endothelial dysfunction. | |
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MedLine Citation:
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PMID: 11751725 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Heart failure is characterized by neurohumoral alterations, such as activation of the sympathetic nervous system, stimulation of the renin-angiotensin system, increased activity of the endothelin system, increased production of norepinephrine, and increased circulating levels of cytokines. Oxidative stress is associated with the formation of reactive oxygen species (ROS). The myocardium has enzymes that stimulate ROS generation and enzymes with antioxidant effects. Several studies have suggested that ROS are increased in the failing heart. ROS may contribute to the pathophysiology of heart failure by initiating myocyte apoptosis and exerting direct negatively inotropic effects through the reduction of cytosolic intracellular free calcium. However, mechanisms such as endothelial dysfunction and inflammation have also been involved in the progression of heart failure. Antioxidants (eg, vitamin C) seem to improve endothelial functionality and reduce the inflammatory response in patients with heart failure. Therefore, in this review, we analyzed the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure. |
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Authors:
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A López Farré; S Casado |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Hypertension Volume: 38 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2001 Dec |
Date Detail:
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Created Date: 2001-12-25 Completed Date: 2002-02-13 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1400-5 Citation Subset: IM |
Affiliation:
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Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain. alopeza@fjd.es |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cardiovascular Agents / pharmacology Endothelium, Vascular / metabolism* Heart Failure / drug therapy, physiopathology* Humans Myocardium / metabolism Neutrophil Activation Nitric Oxide Synthase / genetics Oxidation-Reduction Oxidative Stress RNA, Messenger / metabolism Reactive Oxygen Species / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Cardiovascular Agents; 0/RNA, Messenger; 0/Reactive Oxygen Species; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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