Document Detail


Heart failure, redox alterations, and endothelial dysfunction.
MedLine Citation:
PMID:  11751725     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
A López Farré; S Casado
Related Documents :
20508205 - Role of heme oxygenase-1 in human endothelial cells: lesson from the promoter allelic v...
7902335 - Carvedilol, a new antihypertensive agent, prevents lipid peroxidation and oxidative inj...
21718615 - In vitro effect of n-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide on differentiatio...
2380255 - Comparative study of oxygen toxicity in human fibroblasts and endothelial cells.
8864745 - Granulosa cells express integrin alpha 6: possible involvement of integrin alpha 6 in f...
24277575 - Integrin-mediated cell surface recruitment of autotaxin promotes persistent directional...
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Hypertension     Volume:  38     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-12-25     Completed Date:  2002-02-13     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1400-5     Citation Subset:  IM    
Affiliation:
Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain. alopeza@fjd.es
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
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:
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


Previous Document:  Oxidative stress in arterial hypertension: role of NAD(P)H oxidase.
Next Document:  Cardiomyocyte apoptotic cell death in arterial hypertension: mechanisms and potential management.