Hemodynamic and metabolic effects of angiotensin II on the liver

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dc.contributor.authorNascimento, T. A.
dc.contributor.authorGioli-Pereira, L.
dc.contributor.authorCarvalho, L. T.
dc.contributor.authorSantos, E. L.
dc.contributor.authorPesquero, J. B.
dc.contributor.authorKouyoumdjian, M.
dc.contributor.authorBorges, D. R.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual de Maringá (UEM)
dc.date.accessioned2016-01-24T12:37:39Z
dc.date.available2016-01-24T12:37:39Z
dc.date.issued2005-02-01
dc.description.abstractTo ascertain the mechanism of interaction between angiotensins (AI and AII) and the liver. an angiotensin-converting enzyme inhibitor (captopril) and a receptor antagonist (losartan) were used. Monovascular or bivascular liver perfusion was used to assess both hemodynamic (portal and arterial hypertensive responses) and metabolic (glucose production and oxygen consumption) effects. Microphysiometry was used for isolated liver cell assays to assess AII or losartan membrane receptor-mediated interaction. Captopril abolishes portal hypertensive response (PHR) to AI but not the AII effect. AII infused via the portal pathway promotes calcium-dependent PHR but not a hypertensive response in the arterial pathway (AHR); when infused into the arterial pathway AII promotes calcium-dependent PHR and AHR. Losartan infused into the portal vein abolishes PHR to AII but not the metabolic response: when infused via both pathways it abolishes the hypertensive responses and inhibits the metabolic effects. Isolated liver cells specifically respond to AII Sinusoidal cells, but not hepatocytes. respond to 10 nM losartan. We conclude that AI has to be converted to AII to produce PHR. Quiescent stellate cells interacts in vitro with AII and losartan. Hemodynamic responses to AII are losartan-dependent but metabolic responses are partially losarian-independent, AII hemodynamic actions are mainly presinusoidal. (C) 2004 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Med, BR-05674011 São Paulo, Brazil
dc.description.affiliationUniv Estadual Maringa, Dept Biochem, Parana, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biochem, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Med, BR-05674011 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biochem, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent315-322
dc.identifierhttp://dx.doi.org/10.1016/j.peptides.2004.09.017
dc.identifier.citationPeptides. New York: Elsevier B.V., v. 26, n. 2, p. 315-322, 2005.
dc.identifier.doi10.1016/j.peptides.2004.09.017
dc.identifier.issn0196-9781
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28141
dc.identifier.wosWOS:000226429700018
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofPeptides
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectangiotensinen
dc.subjectangiotensin-converting enzymeen
dc.subjectbivascular liver perfusionen
dc.subjectportal hypertensionen
dc.subjectangiotensin receptoren
dc.subjectlosartanen
dc.titleHemodynamic and metabolic effects of angiotensin II on the liveren
dc.typeinfo:eu-repo/semantics/article
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