| Progressive cardiac hypertrophy and dysfunction in atrial natriuretic peptide receptor (GC-A) deficient mice. | |
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MedLine Citation:
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PMID: 11907014 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: To investigate how permanent inhibition of guanylyl cyclase A receptor (GC-A) affects cardiac function. METHODS: Hearts of GC-A-/- and corresponding wild type mice (GC-A+/+) were characterised by histological, western blotting, and northern blotting analyses. Cardiac function was evaluated in isolated, working heart preparations. RESULTS: At 4 months of age, GC-A-/- mice had global cardiac hypertrophy (about a 40% increase in cardiac weight) without interstitial fibrosis. Examination of heart function found a significant delay in the time of relaxation; all other parameters of cardiac contractility were similar to those in wild type mice. At 12 months, the hypertrophic changes were much more severe (about a 61% increase in cardiac weight), together with a shift in cardiac gene expression (enhanced concentrations of atrial natriuretic peptide (3.8-fold), B type natriuretic peptide (2-fold), beta myosin heavy chain (1.6-fold) and alpha skeletal actin (1.7-fold) mRNA), increased expression of cytoskeletal tubulin and desmin (by 29.6% and 25.6%, respectively), and pronounced interstitial fibrosis. These changes were associated with significantly impaired cardiac contractility (+dP/dt decreased by about 10%) and relaxation (-dP/dt decreased by 21%), as well as depressed contractile responses to pressure load (all p < 0.05). CONCLUSIONS: Chronic hypertension in GC-A-/- mice is associated with progressive cardiac changes--namely, initially compensated cardiomyocyte hypertrophy, which is complicated by interstitial fibrosis and impaired cardiac contractility at later stages. |
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Authors:
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M Kuhn; R Holtwick; H A Baba; J C Perriard; W Schmitz; E Ehler |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Heart (British Cardiac Society) Volume: 87 ISSN: 1468-201X ISO Abbreviation: Heart Publication Date: 2002 Apr |
Date Detail:
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Created Date: 2002-03-21 Completed Date: 2002-04-16 Revised Date: 2013-06-09 |
Medline Journal Info:
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Nlm Unique ID: 9602087 Medline TA: Heart Country: England |
Other Details:
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Languages: eng Pagination: 368-74 Citation Subset: AIM; IM |
Affiliation:
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Institute of Pharmacology and Toxicology, Westfälische Wilhelms-Universität Münster, Münster, Germany. mkuhn@uni-muenster.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / physiology Blotting, Northern Blotting, Western Cardiomegaly / etiology*, pathology, physiopathology Endomyocardial Fibrosis / etiology Guanylate Cyclase* Hypertension / etiology Immunohistochemistry Male Mice Receptors, Atrial Natriuretic Factor* Receptors, Cell Surface / deficiency* Ventricular Function, Left / physiology |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Cell Surface; EC 4.6.1.2/Guanylate Cyclase; EC 4.6.1.2/Receptors, Atrial Natriuretic Factor; EC 4.6.1.2/atrial natriuretic factor receptor A |
| Comments/Corrections | |
Comment In:
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Heart. 2002 Apr;87(4):314-5
[PMID:
11906995
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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