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Authordc.contributor.authorOcaranza, Maria Paz 
Authordc.contributor.authorLavandero González, Sergio 
Authordc.contributor.authorJalil Milad, Jorge 
Authordc.contributor.authorMoya, Jaqueline 
Authordc.contributor.authorPinto, Melissa 
Authordc.contributor.authorNovoa, Ulises 
Authordc.contributor.authorApablaza, Felipe 
Authordc.contributor.authorGonzález, Leticia 
Authordc.contributor.authorHernández, Carol 
Authordc.contributor.authorVaras, Manuel 
Authordc.contributor.authorLópez, René 
Authordc.contributor.authorGodoy, Iván 
Authordc.contributor.authorVerdejo, Hugo 
Authordc.contributor.authorChiong Lay, Mario 
Cita de ítemdc.identifier.citationJournal of Hypertension, Volumen 28, Issue 5, 2010, Pages 1054-1064
Abstractdc.description.abstractBackground: Angiotensin-(1-9) is present in human and rat plasma and its circulating levels increased early after myocardial infarction or in animals treated with angiotensin-converting enzyme inhibitor. However, the cardiovascular effects of this peptide are unknown. Objective: To determine whether angiotensin-(1-9) is a novel anti-cardiac hypertrophy factor in vitro and in vivo and whether this peptide is involved in the pharmacological effects of cardiovascular drugs acting on the renin-angiotensin system. Methods and results The administration of angiotensin(1-9) to myocardial infarcted rats by osmotic minipumps (450 ng/kg per min, n=6) vs. vehicle (n=8) for 2 weeks decreased plasma angiotensin II levels, inhibited angiotensin- converting enzyme activity and also prevented cardiac myocyte hypertrophy. However, cardiac myocyte hypertrophy attenuation triggered by angiotensin-(1-9) was not modified with the simultaneous administration of the angiotensin-(1-7) receptor antagonist A779 (100 ng/kg per min, n=6). In experiments in vitro with cultured cardiac myocytes incubated with norepinephrine (10 mu mol/l) or with insulin-like growth factor-1 (10 nmol/l), angiotensin(1-9) also prevented hypertrophy. In other experimental setting, myocardial infarcted rats (n=37) were randomized to receive either vehicle (n=12), enalapril (10 mg/kg per day, n=12) or angiotensin II receptor blocker candesartan (10 mg/kg per day, n=13) for 8 weeks. Both drugs prevented left ventricle hypertrophy and increased plasma angiotensin-(1-9) levels by several folds. Angiotensin-(1-9) levels correlated negatively with different left ventricular hypertrophy markers even after adjustment for blood pressure reduction. Conclusion Angiotensin-(1-9) is an effective and a novel anti-cardiac hypertrophy agent not acting via the Mas receptor.
Publisherdc.publisherLippincott Williams and Wilkins
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.uri
Sourcedc.sourceJournal of Hypertension
Keywordsdc.subjectAngiotensin-converting enzyme 2
Keywordsdc.subjectCardiac dysfunction
Keywordsdc.subjectCardiac hypertrophy
Keywordsdc.subjectCardiac myocyte
Keywordsdc.subjectMyocardial infarction
Títulodc.titleAngiotensin-(1-9) regulates cardiac hypertrophy in vivo and in vitro
Document typedc.typeArtículo de revista
Indexationuchile.indexArtículo de publicación SCOPUS

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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile