Document Detail


Reactive oxygen species and vascular biology: implications in human hypertension.
MedLine Citation:
PMID:  20981034     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.
Authors:
Rhian M Touyz; Ana M Briones
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-28
Journal Detail:
Title:  Hypertension research : official journal of the Japanese Society of Hypertension     Volume:  34     ISSN:  1348-4214     ISO Abbreviation:  Hypertens. Res.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-05     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  5-14     Citation Subset:  IM    
Affiliation:
Kidney Research Centre, Ottawa Health Research Institute, University of Ottawa, Ottawa, Ontario, Canada. rtouyz@uottawa.ca
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
44018//Canadian Institutes of Health Research; 57886//Canadian Institutes of Health Research

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