Document Detail


Angiotensin-(1-7) ameliorates myocardial remodeling and interstitial fibrosis in spontaneous hypertension: role of MMPs/TIMPs.
MedLine Citation:
PMID:  20837116     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Angiotensin-(1-7) displays antihypertensive and antiproliferative properties although its effect on cardiac remodeling and hypertrophy in hypertension has not been fully elucidated. The present study was designed to examine the effect of chronic angiotensin-(1-7) treatment on myocardial remodeling, cardiac hypertrophy and underlying mechanisms in spontaneous hypertension. Adult male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were treated with or without angiotensin-(1-7) or the angiotensin-(1-7) antagonist A-779 for 24 weeks. Mean arterial pressure, left ventricular geometry, expression of the hypertrophic markers ANP and β-MHC, collagen contents (type I and III), collagenase (MMP-1), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of MMPs-1 (TIMP-1) were evaluated in WKY and SHR rats with or without treatment. Our data revealed that chronic angiotensin-(1-7) treatment significantly suppressed hypertension, left ventricular hypertrophy, expression of ANP and β-MHC as well as myocardial fibrosis in SHR rats, the effects of which were nullified by the angiotensin-(1-7) receptor antagonist A-779. In addition, angiotensin-(1-7) treatment significantly counteracted hypertension-induced changes in the mRNA expression of MMP-2 and TIMP-1 and collagenase activity, the effects of which were blunted by A-779. In vitro study revealed that angiotensin-(1-7) directly increased the activity of MMP-2 and MMP-9 while decreasing the content of TIMP-1 and TIMP-2. Taken together, our results revealed a protective effect of angiotensin-(1-7) against cardiac hypertrophy and collagen deposition, which may be related to concerted changes in MMPs and TIMPs levels. These data indicated the therapeutic potential of angiotensin-(1-7) in spontaneous hypertension-induced cardiac remodeling.
Authors:
Zhaohui Pei; Rongsen Meng; Guangwei Li; Guangmei Yan; Changqing Xu; Zhiqiang Zhuang; Jun Ren; Zhenbiao Wu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-17
Journal Detail:
Title:  Toxicology letters     Volume:  199     ISSN:  1879-3169     ISO Abbreviation:  Toxicol. Lett.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-18     Completed Date:  2010-11-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7709027     Medline TA:  Toxicol Lett     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  173-81     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Department of Cardiology, The Third Hospital, Nanchang, Jiangxi, China.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin I / pharmacology*
Animals
Antihypertensive Agents / pharmacology*
Atrial Natriuretic Factor / analysis,  genetics
Blood Pressure / drug effects
Cardiomegaly / prevention & control*
Collagen / metabolism
Collagenases / metabolism
Fibrosis
Hypertension / drug therapy*,  metabolism,  pathology
Male
Matrix Metalloproteinase 2 / analysis,  physiology*
Matrix Metalloproteinase 9 / analysis,  physiology*
Myocardium / metabolism,  pathology*
Myosin Heavy Chains / analysis,  genetics
Peptide Fragments / pharmacology*
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Tissue Inhibitor of Metalloproteinases / analysis,  physiology*
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Bmyo protein, rat; 0/Myosin Heavy Chains; 0/Peptide Fragments; 0/Tissue Inhibitor of Metalloproteinases; 0/angiotensin I (1-7); 85637-73-6/Atrial Natriuretic Factor; 9007-34-5/Collagen; 9041-90-1/Angiotensin I; EC 3.4.24.-/Collagenases; EC 3.4.24.24/Matrix Metalloproteinase 2; EC 3.4.24.35/Matrix Metalloproteinase 9

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