Document Detail

Temporal regulation of extracellular matrix components in transition from compensatory hypertrophy to decompensatory heart failure.
MedLine Citation:
PMID:  10067796     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Extracellular matrix, particularly type I fibrillar collagen, provides tensile strength that allows cardiac muscle to perform systolic and diastolic functions. Collagen is induced during the transition from compensatory hypertrophy to heart failure. We hypothesized that cardiac stiffness during decompensatory hypertrophy is partly due to a decreased elastin:collagen ratio. MATERIALS AND METHODS: We prepared left ventricular tissue homogenates from spontaneously hypertensive rats (SHR) aged 30-36 weeks, which had compensatory hypertrophy with no heart failure, and from SHR aged 70-92 weeks, which had decompensatory hypertrophy with heart failure. Age- and sex-matched Wistar-Kyoto (WKY) rats were used as normotensive controls. In both SHR groups, increased levels of collagen were detected by immuno-blot analysis using type I collagen antibody. Elastin and collagen were quantitated by measuring desmosine/isodesmosine and hydroxyproline spectrophometrically, respectively. To determine whether the decrease in elastin content was due to increased elastinolytic activity of matrix metalloproteinase-2, we performed gelatin and elastin zymography on left ventricular tissue homogenates from control rats, SHR with compensatory hypertrophy and SHR with heart failure. RESULTS: The elastin:collagen ratio was 0.242 +/- 0.008 in hearts from WKY rats. In SHR without heart failure, the ratio was decreased to 0.073 +/- 0.003 and in decompensatory hypertrophy with heart failure, the ratio decreased to 0.012 +/- 0.005. Matrix metalloproteinase-2 activity was increased significantly in SHR with heart failure compared with controls (P < 0.001). The level of tissue inhibitor of metalloproteinase-4 was increased in compensatory hypertrophy and markedly reduced in heart failure. Decorin was strongly reduced in decompensatory heart failure compared with control hearts. CONCLUSIONS: Since collagen was induced in SHR with heart failure, decorin and elastin were decreased and the ratios of gelatinase A and elastase to tissue inhibitor of metalloproteinase-4 were increased, we conclude that heart failure is associated with adverse extracellular matrix remodeling.
V S Mujumdar; S C Tyagi
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of hypertension     Volume:  17     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-04-28     Completed Date:  1999-04-28     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  261-70     Citation Subset:  IM    
Department of Physiology and Biophysics, and Center of Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson 39216-4505, USA.
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MeSH Terms
Blotting, Western
Collagen / metabolism*
Disease Models, Animal
Disease Progression
Elastin / metabolism*
Extracellular Matrix / metabolism*
Extracellular Matrix Proteins
Follow-Up Studies
Gelatinases / metabolism
Heart Failure / etiology,  metabolism*,  physiopathology
Heart Ventricles / metabolism*,  pathology,  physiopathology
Hypertrophy, Left Ventricular / complications,  metabolism*,  physiopathology
Matrix Metalloproteinase 2
Metalloendopeptidases / metabolism
Myocardial Contraction
Proteoglycans / metabolism
Rats, Inbred SHR
Rats, Inbred WKY
Tensile Strength
Tissue Inhibitor of Metalloproteinases / metabolism
Transforming Growth Factor beta / antagonists & inhibitors
Grant Support
Reg. No./Substance:
0/Extracellular Matrix Proteins; 0/Proteoglycans; 0/Tissue Inhibitor of Metalloproteinases; 0/Transforming Growth Factor beta; 0/decorin; 9007-34-5/Collagen; 9007-58-3/Elastin; EC 3.4.24.-/Gelatinases; EC 3.4.24.-/Metalloendopeptidases; EC Metalloproteinase 2

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

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