| Role of the B1 kinin receptor in the regulation of cardiac function and remodeling after myocardial infarction. | |
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MedLine Citation:
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PMID: 15699461 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Kinins exert cardioprotective effects via 2 G-protein-coupled receptors, B1 and B2. Using B1 kinin receptor gene knockout mice (B1-/-), we tested the hypotheses that the B1 receptor plays an important role in preservation of cardiac function, whereas lack of B1 may accelerate cardiac remodeling and dysfunction after myocardial infarction, and that B2 receptors may compensate for lack of B1, whereas blockade of B2 receptors in B1-/- mice may cause further deterioration of cardiac function and remodeling. Female B1-/- mice and wild-type controls (C57BL/6J, B1+/+) underwent sham surgery or myocardial infarction and were treated with either vehicle or B2-antagonist (icatibant, 500 microg/kg per day, subcutaneous) for 8 weeks. We found that in sham myocardial infarction, B1-/- mice had a larger left ventricular diastolic chamber dimension both initially and at 4 to 8 weeks compared with B1+/+. Left ventricular mass and myocyte size were also larger in B1-/- with sham operation than in B1+/+, although cardiac function did not differ between strains. After myocardial infarction, cardiac remodeling and function were similar in both strains, although B1-/- mice tended to have lower blood pressure. Blockade of B2 receptors tended to worsen cardiac remodeling and dysfunction in B1-/- but not in B1+/+. These results may suggest that B2 receptors play an important role in compensating for lack of B1 receptors in mice with myocardial infarction. Dual blockade of both B1 and B2 eliminates this compensation, leading to further deterioration of cardiac dysfunction and remodeling after myocardial infarction. |
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Authors:
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Jiang Xu; Oscar A Carretero; Ying Sun; Edward G Shesely; Nour-Eddine Rhaleb; Yun-He Liu; Tang-Dong Liao; James J Yang; Michael Bader; Xiao-Ping Yang |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2005-02-07 |
Journal Detail:
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Title: Hypertension Volume: 45 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2005 Apr |
Date Detail:
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Created Date: 2005-03-25 Completed Date: 2005-10-27 Revised Date: 2007-11-14 |
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: 747-53 Citation Subset: IM |
Affiliation:
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Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich 48202-2689, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / drug effects Bradykinin / pharmacology Female Heart / physiopathology* Heart Rate Heart Ventricles Mice Mice, Inbred C57BL Mice, Knockout Myocardial Infarction / mortality, pathology, physiopathology* Myocardium / metabolism*, pathology Organ Size Receptor, Bradykinin B1 / deficiency, metabolism* Receptor, Bradykinin B2 / antagonists & inhibitors Systole Ventricular Remodeling* |
| Grant Support | |
ID/Acronym/Agency:
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HL-28982/HL/NHLBI NIH HHS; HL-71806/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptor, Bradykinin B1; 0/Receptor, Bradykinin B2; 58-82-2/Bradykinin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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