Document Detail

Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice.
MedLine Citation:
PMID:  18180400     Owner:  NLM     Status:  MEDLINE    
Mas codes for a G protein-coupled receptor that is implicated in angiotensin-(1-7) signaling. We studied the cardiovascular phenotype of Mas-deficient mice backcrossed onto the FVB/N genetic background using telemetry and found that they exhibit higher blood pressures compared with controls. These Mas(-/-) mice also had impaired endothelial function, decreased NO production, and lower endothelial NO synthase expression. Reduced nicotinamide-adenine dinucleotide phosphate oxidase catalytic subunit gp91(phox) protein content determined by Western blotting was higher in Mas(-/-) mice than in controls, whereas superoxide dismutase and catalase activities were reduced. The superoxide dismutase mimetic, Tempol, decreased blood pressure in Mas(-/-) mice but had a minimal effect in control mice. Our results show a major cardiovascular phenotype in Mas(-/-) mice. Mas-deletion results in increased blood pressure, endothelial dysfunction, and an imbalance between NO and reactive oxygen species. Our animals represent a promising model to study angiotensin-(1-7)-mediated cardiovascular effects and to evaluate Mas agonistic compounds as novel cardioprotective and antihypertensive agents based on their beneficial effects on endothelial function.
Ping Xu; Andrey C Costa-Goncalves; Mihail Todiras; Luiza A Rabelo; Walkyria O Sampaio; Marina M Moura; Sergio Sousa Santos; Friedrich C Luft; Michael Bader; Volkmar Gross; Natalia Alenina; Robson A S Santos
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-07
Journal Detail:
Title:  Hypertension     Volume:  51     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-01-24     Completed Date:  2008-02-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  574-80     Citation Subset:  IM    
Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Str 10, D-13125 Berlin-Buch, Germany.
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MeSH Terms
Antioxidants / pharmacology
Aorta / metabolism
Biological Availability
Blood Pressure* / drug effects
Blotting, Western
Cyclic N-Oxides / pharmacology
Endothelium, Vascular / physiopathology*
Membrane Glycoproteins
Mice, Inbred Strains
Mice, Knockout
NADPH Oxidase
Nitric Oxide / metabolism
Oxidative Stress
Proto-Oncogene Proteins / deficiency*
Reactive Oxygen Species / metabolism
Receptors, G-Protein-Coupled / deficiency*
Spin Labels
Reg. No./Substance:
0/Antioxidants; 0/Cyclic N-Oxides; 0/Membrane Glycoproteins; 0/Proto-Oncogene Proteins; 0/Reactive Oxygen Species; 0/Receptors, G-Protein-Coupled; 0/Spin Labels; 0/proto-oncogene proteins c-mas-1; 10102-43-9/Nitric Oxide; 2226-96-2/tempol; EC protein, mouse; EC Oxidase

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

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