Document Detail


Renal oxidative stress, oxygenation, and hypertension.
MedLine Citation:
PMID:  21832206     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertension is closely associated with progressive kidney dysfunction, manifested as glomerulosclerosis, interstitial fibrosis, proteinuria, and eventually declining glomerular filtration. The postulated mechanism for development of glomerulosclerosis is barotrauma caused by increased capillary pressure, but the reason for development of interstitial fibrosis and the subsequently reduced kidney function is less clear. However, it has been hypothesized that tissue hypoxia induces fibrogenesis and progressive renal failure. This is very interesting, since recent reports highlight several different mechanisms resulting in altered oxygen handling and availability in the hypertensive kidney. Such mechanisms include decreased renal blood flow due to increased vascular tone induced by ANG II that limits oxygen delivery and increases oxidative stress, resulting in increased mitochondrial oxygen usage, increased oxygen usage for tubular electrolyte transport, and shunting of oxygen from arterial to venous blood in preglomerular vessels. It has been shown in several studies that interventions to prevent oxidative stress and to restore kidney tissue oxygenation prevent progression of kidney dysfunction. Furthermore, inhibition of ANG II activity, by either blocking ANG II type 1 receptors or angiotensin-converting enzyme, or by preventing oxidative stress by administration of antioxidants also results in improved blood pressure control. Therefore, it seems likely that tissue hypoxia in the hypertensive kidney contributes to progression of kidney damage, and perhaps also persistence the high blood pressure.
Authors:
Fredrik Palm; Lina Nordquist
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-08-10
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  301     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-03     Completed Date:  2011-12-22     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1229-41     Citation Subset:  IM    
Affiliation:
Dept. of Medical Cell Biology, Uppsala Univ., Biomedical Center, Box 571, 751 23 Uppsala, Sweden. Fredrik.Palm@mcb.uu.se
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism
Animals
Anoxia / metabolism
Antioxidants / metabolism,  therapeutic use
Disease Progression
Fibrosis
Humans
Hypertension / drug therapy,  metabolism*,  pathology,  physiopathology
Kidney / drug effects,  metabolism*,  pathology,  physiopathology
Kidney Diseases / drug therapy,  metabolism*,  pathology,  physiopathology
Oxidative Stress*
Oxygen / metabolism*
Oxygen Consumption*
Reactive Oxygen Species / metabolism
Grant Support
ID/Acronym/Agency:
K99/R00/DK077858/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 11128-99-7/Angiotensin II; 7782-44-7/Oxygen
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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