Document Detail


Pressure overload causes cardiac hypertrophy in beta1-adrenergic and beta2-adrenergic receptor double knockout mice.
MedLine Citation:
PMID:  16467660     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Cardiac hypertrophy arises as an adaptive response to increased afterload. Studies in knockout mice have shown that catecholamines, but not alpha1-adrenergic receptors, are necessary for such an adaptation to occur. However, whether beta-adrenergic receptors are critical for the development of cardiac hypertrophy in response to pressure overload is not known at this time. METHODS AND RESULTS: Pressure overload was induced by transverse aortic banding in beta1-adrenergic and beta2-adrenergic receptor double knockout (DbetaKO) mice, in which the predominant cardiac beta-adrenergic receptor subtypes are lacking. Chronic pressure overload for 4 weeks induced cardiac hypertrophy in both DbetaKO and wild-type mice. There were no significant differences between banded mice in left ventricular weight to body weight ratio, in the left ventricular wall thickness, in the cardiomyocyte size or in the expression levels of the load-sensitive cardiac genes such as ANF and beta-MHC. Additionally, the left ventricular systolic pressure, an index of afterload, and cardiac contractility, evaluated as dp/dtmax, the maximal slope of systolic pressure increment, and Ees, end-systolic elastance, were increased at a similar level in both wild-type and DbetaKO banded mice, and were significantly greater than in sham controls. CONCLUSION: Despite chronic activation of the cardiac beta-adrenergic system being sufficient to induce a pathological hypertrophy, we show that beta1-adrenergic and beta2-adrenergic receptors are not an obligatory component of the signaling pathway that links the increased afterload to the development of cardiac hypertrophy.
Authors:
Sergio Palazzesi; Marco Musumeci; Liviana Catalano; Mario Patrizio; Tonino Stati; Simona Michienzi; Maria Grazia Di Certo; Elisabetta Mattei; Luigi Vitelli; Giuseppe Marano
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  24     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-02-09     Completed Date:  2006-05-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  563-71     Citation Subset:  IM    
Affiliation:
Department of Drug Research and Evaluation, Istituto Superiore di Sanità, Consiglio Nazionale delle Ricerche, Rome, Italy.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Blood Pressure
Gene Expression Regulation
Heart / physiology
Heart Ventricles / pathology
Hypertrophy, Left Ventricular / etiology,  pathology,  physiopathology*
Male
Mice
Mice, Knockout
Myocytes, Cardiac / pathology
Receptors, Adrenergic, beta-1 / physiology*
Receptors, Adrenergic, beta-2 / physiology*
Renin-Angiotensin System
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic, beta-1; 0/Receptors, Adrenergic, beta-2

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


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