Document Detail


Effects of genetic deletion of angiotensin-(1-7) receptor Mas on cardiac function during ischemia/reperfusion in the isolated perfused mouse heart.
MedLine Citation:
PMID:  17055538     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In this study we investigated the role of Mas on cardiac function during ischemia/reperfusion in isolated perfused mouse heart. Following a stabilization period of 30 min, hearts from WT and Mas KO mice were subjected to global ischemia. After 20 min of ischemia, the flow was restarted and the hearts were reperfused for 30 min. An additional group of WT mice was perfused with solution containing the Ang-(1-7) receptor Mas antagonist A-779. Isolated heart of Mas KO and WT treated with A-779 presented an increase in the perfusion pressure in the baseline period. This difference increased with 5 min of reperfusion reaching similar values to baseline period at the end of the reperfusion. Isolated hearts of Mas KO and WT treated with A-779 also presented a decreased systolic tension, +/-dT/dt, and HR. Upon global ischemia WT hearts showed a significant decrease in systolic tension and an increase in diastolic tension. During reperfusion an increase in systolic and diastolic tension was observed in WT mice. Deletion or blockade of Mas markedly attenuated these changes in isolated hearts. These results indicate that Mas plays an important role in cardiac function during ischemia/reperfusion which is in keeping with the cardiac and coronary effects previously described for Ang-(1-7).
Authors:
Carlos H Castro; Robson A S Santos; Anderson J Ferreira; Michael Bader; Natalia Alenina; Alvair P Almeida
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-09-16
Journal Detail:
Title:  Life sciences     Volume:  80     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-02-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  264-8     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin I / antagonists & inhibitors
Angiotensin II / analogs & derivatives*,  pharmacology
Animals
Diastole / drug effects
Mice
Mice, Knockout
Myocardial Ischemia / genetics,  physiopathology*
Peptide Fragments / antagonists & inhibitors,  pharmacology*
Proto-Oncogene Proteins / deficiency*
Receptors, G-Protein-Coupled / deficiency*
Reperfusion
Systole / drug effects
Chemical
Reg. No./Substance:
0/7-Ala-angiotensin (1-7); 0/Peptide Fragments; 0/Proto-Oncogene Proteins; 0/Receptors, G-Protein-Coupled; 0/angiotensin I (1-7); 0/proto-oncogene proteins c-mas-1; 11128-99-7/Angiotensin II; 9041-90-1/Angiotensin I

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


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