| Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice. | |
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MedLine Citation:
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PMID: 18180400 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-01-07 |
Journal Detail:
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Title: Hypertension Volume: 51 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-01-24 Completed Date: 2008-02-26 Revised Date: - |
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: 574-80 Citation Subset: IM |
Affiliation:
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Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Str 10, D-13125 Berlin-Buch, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / pharmacology Aorta / metabolism Biological Availability Blood Pressure* / drug effects Blotting, Western Cyclic N-Oxides / pharmacology Endothelium, Vascular / physiopathology* Male Membrane Glycoproteins Mice Mice, Inbred Strains Mice, Knockout NADPH Oxidase Nitric Oxide / metabolism Oxidative Stress Phenotype Proto-Oncogene Proteins / deficiency* Reactive Oxygen Species / metabolism Receptors, G-Protein-Coupled / deficiency* Spin Labels Vasodilation* |
| Chemical | |
Reg. No./Substance:
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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 1.6.3.1/Cybb protein, mouse; EC 1.6.3.1/NADPH Oxidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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