Enalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat

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dc.contributor.authorOcaranza, Maria Paz
dc.contributor.authorGodoy, Ivan
dc.contributor.authorJalil, Jorge E.
dc.contributor.authorVaras, Manuel
dc.contributor.authorCollantes, Patricia
dc.contributor.authorPinto, Melissa
dc.contributor.authorRoman, Maritza
dc.contributor.authorRamirez, Cristian
dc.contributor.authorCopaja, Miguel
dc.contributor.authorDiaz Araya, Guillermo
dc.contributor.authorCastro, Pablo
dc.contributor.authorLavandero, Sergio
dc.date.accessioned2024-01-10T13:48:00Z
dc.date.available2024-01-10T13:48:00Z
dc.date.issued2006
dc.description.abstractThe early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfafction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.
dc.fechaingreso.objetodigital2024-05-16
dc.format.extent7 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1161/01.HYP.0000237862.94083.45
dc.identifier.eissn1524-4563
dc.identifier.issn0194-911X
dc.identifier.pubmedidMEDLINE:16908757
dc.identifier.urihttps://doi.org/10.1161/01.HYP.0000237862.94083.45
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79325
dc.identifier.wosidWOS:000243571200015
dc.information.autorucMedicina;Castro P;S/I;100212
dc.information.autorucMedicina;Jalil J;S/I;99946
dc.information.autorucMedicina;Ocaranza M;S/I;1001254
dc.issue.numero4
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final578
dc.pagina.inicio572
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.revistaHYPERTENSION
dc.rightsacceso restringido
dc.subjectangiotensin-converting enzyme
dc.subjectmyocardial infafction
dc.subjectrenin-angiotensin system
dc.subjectremodeling
dc.subjectcardiac function
dc.subjectHEART FUNCTION
dc.subjectCARBOXYPEPTIDASE ACE2
dc.subjectRECEPTOR BLOCKADE
dc.subjectGENE-EXPRESSION
dc.subjectINHIBITION
dc.subjectBRADYKININ
dc.subjectPROTEIN
dc.subjectHYPERTROPHY
dc.subjectMETABOLISM
dc.subjectCAPTOPRIL
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEnalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat
dc.typeartículo
dc.volumen48
sipa.codpersvinculados100212
sipa.codpersvinculados99946
sipa.codpersvinculados1001254
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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