Document Detail

Angiotensin-(1-7) improves cardiac remodeling and inhibits growth-promoting pathways in the heart of fructose-fed rats.
MedLine Citation:
PMID:  20061544     Owner:  NLM     Status:  MEDLINE    
The present study examined whether chronic treatment with angiotensin (ANG)-(1-7) reduces cardiac remodeling and inhibits growth-promoting signaling pathways in the heart of fructose-fed rats (FFR), an animal model of insulin resistance. Sprague-Dawley rats were fed either normal rat chow (control) or the same diet plus 10% fructose in drinking water. For the last 2 wk of a 6-wk period of the corresponding diet, control and FFR were implanted with osmotic pumps that delivered ANG-(1-7) (100 A subgroup of each group of animals (control or FFR) underwent a sham surgery. We determined heart weight, myocyte diameter, interstitial fibrosis, and perivascular collagen type III deposition as well as the phosphorylation degree of ERK1/2, JNK1/2, and p38MAPK. FFR showed a mild hypertension that was significantly reduced after ANG-(1-7) treatment. Also, FFR displayed higher ANG II circulating and local levels in the heart that remained unaltered after chronic ANG-(1-7) infusion. An increased heart-to-body weight ratio, myocyte diameter, as well as left ventricular fibrosis and perivascular collagen type III deposition were detected in the heart of FFR. Interestingly, significant improvements in these cardiac alterations were obtained after ANG-(1-7) treatment. Finally, FFR that received ANG-(1-7) chronically displayed significantly lower phosphorylation levels of ERK1/2, JNK1/2, and p38MAPK. The beneficial effects obtained by ANG-(1-7) were associated with normal values of Src-homology 2-containing protein-tyrosine phosphatase-1 (SHP-1) activity in the heart. In conclusion, chronic ANG-(1-7) treatment ameliorated cardiac hypertrophy and fibrosis and attenuated the growth-promoting pathways in the heart. These findings show an important protective role of ANG-(1-7) in the heart of insulin-resistant rats.
Jorge F Giani; Marina C Mu?oz; Marcos A Mayer; Luciana C Veiras; Cristina Arranz; Carlos A Taira; Daniel Turyn; Jorge E Toblli; Fernando P Dominici
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-08
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-25     Completed Date:  2010-04-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1003-13     Citation Subset:  IM    
Instituto de Qu?mica y Fisicoqu?mica Biol?gicas, Universidad de Buenos Aires-Consejo Nacional de Investigaciones Cient?ficas y Tecnol?gicas of Argentina, Argentina.
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MeSH Terms
Angiotensin I / pharmacology*
Angiotensin II / metabolism
Antihypertensive Agents / pharmacology
Blood Pressure / physiology
Dietary Carbohydrates / adverse effects
Disease Models, Animal
Fructose / adverse effects*
Hypertension / etiology,  metabolism,  physiopathology*
Hypertrophy, Left Ventricular / etiology,  physiopathology,  prevention & control*
Insulin / blood
Insulin Resistance*
Peptide Fragments / pharmacology*
Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism
Rats, Sprague-Dawley
Ventricular Remodeling / drug effects*
Reg. No./Substance:
0/Antihypertensive Agents; 0/Dietary Carbohydrates; 0/Peptide Fragments; 0/angiotensin I (1-7); 11061-68-0/Insulin; 11128-99-7/Angiotensin II; 30237-26-4/Fructose; 9041-90-1/Angiotensin I; EC Tyrosine Phosphatase, Non-Receptor Type 6; EC protein, rat

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