| Overexpression of alpha1B-adrenergic receptor induces left ventricular dysfunction in the absence of hypertrophy. | |
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MedLine Citation:
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PMID: 9746484 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The stimulation of cardiac alpha1-adrenergic receptors (AR) modulates the heart's inotropic response and plays a role in the induction of cardiomyocyte hypertrophy. We have analyzed transgenic mouse lines overexpressing a wild-type alpha1B-AR specifically in the heart. Basal level systolic and diastolic left ventricular (LV) contractile function was depressed both in the anesthetized closed-chest mouse and the perfused working-heart preparation. Intrinsic LV function was further characterized under controlled preload and afterload conditions using the perfusion model. Contractile parameters were restored by chronic treatment with the alpha-AR antagonist prazosin. In ventricular function curves, the load-dependent force increases (length-tension effects) remained intact, although the transgenic curve was shifted to lower levels. The basal level contractile deficits were paralleled by a decrease in calcium transients in isolated LV cardiomyocytes. LV function comparable to controls was restored by isoproterenol stimulation. The physiological changes occurred in the absence of cardiomyocyte hypertrophy. This transgenic model will be useful for studying the potential role of alpha1-AR in cardiac contractility and hypertrophy. |
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Authors:
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I L Grupp; J N Lorenz; R A Walsh; G P Boivin; H Rindt |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of physiology Volume: 275 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1998 Oct |
Date Detail:
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Created Date: 1998-11-19 Completed Date: 1998-11-19 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: H1338-50 Citation Subset: IM |
Affiliation:
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Department of Pharmacology and Cell Biophysics, University of Cincinnati, Cincinnati, Ohio 45267, 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 Calcium / metabolism Cardiomegaly / physiopathology* Cells, Cultured Heart / physiology, physiopathology* Heart Rate / drug effects Isoproterenol / pharmacology Mice Mice, Inbred C57BL Mice, Inbred Strains Mice, Transgenic Myocardial Contraction / drug effects, physiology* Myocardium / metabolism, ultrastructure Prazosin / pharmacology Receptors, Adrenergic, alpha-1 / antagonists & inhibitors, genetics, physiology* Regression Analysis Ventricular Dysfunction, Left / physiopathology* Ventricular Function, Left / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Adrenergic, alpha-1; 0/adrenergic receptor alpha(1b); 19216-56-9/Prazosin; 7440-70-2/Calcium; 7683-59-2/Isoproterenol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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