Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B-2-type receptors

dc.contributor.authorLoureiro-Silva, M. R.
dc.contributor.authorMolina, H. M.
dc.contributor.authorBorges, D. R.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:31:15Z
dc.date.available2016-01-24T12:31:15Z
dc.date.issued2001-01-01
dc.description.abstractBackground: We have shown that the portal hypertensive response to bradykinin in normal rats is mediated by B-2 receptors.Methods: By using isolated and exsanguinated rat liver perfusion, we studied the portal hypertensive response to bradykinin or des-Arg(9)-bradykinin (B-1 agonist) in inflamed or cirrhotic rat livers. Livers were perfused with bovine serum albumin Krebs-Henseleit buffer (pH 7.4; 37 degreesC) at a constant flow rate, in the absence or presence of des-Arg(9)[Leu(8)]-bradykinin or HOE 140 (B-1 and B-2 receptor antagonists, respectively). Bradykinin (140 nmol) or des-Arg(9)-bradykinin was injected as a bolus via the afferent route to the liver.Results: Basal perfusion pressure in liver-cirrhotic rats was higher than in normal rats. in normal, inflamed, or liver-cirrhotic rats, the presence of the B-1 antagonist did not change the portal hypertensive response to bradykinin, while the B-2 antagonist abolished this response. A 140-nmol dose of des-Arg(9)-bradykinin did not change the perfusion pressure; 700 nmol of this B-1 agonist produced an insignificant perfusion pressure increase. the perfusion pressure increase induced by bradykinin in cirrhotic livers was lower than in normal livers.Conclusions: the portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B-2 receptors, but not B-1 receptors, and there is a contracting hyporeactivity to bradykinin in cirrhotic rat livers. (C) 2001 Blackwell Science Asia Pty Ltd.en
dc.description.affiliationUniversidade Federal de São Paulo, Lab Expt Hepatol Nucleo Metab Hepat, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Lab Expt Hepatol Nucleo Metab Hepat, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent41-45
dc.identifierhttp://dx.doi.org/10.1046/j.1440-1746.2001.02397.x
dc.identifier.citationJournal of Gastroenterology and Hepatology. Carlton: Blackwell Science Asia, v. 16, n. 1, p. 41-45, 2001.
dc.identifier.doi10.1046/j.1440-1746.2001.02397.x
dc.identifier.issn0815-9319
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/26453
dc.identifier.wosWOS:000167674800007
dc.language.isoeng
dc.publisherBlackwell Science Asia
dc.relation.ispartofJournal of Gastroenterology and Hepatology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectacute phase responseen
dc.subjectbradykinin antagonisten
dc.subjectbradykinin receptoren
dc.subjectbradykininen
dc.subjectcirrhosisen
dc.subjectdes-Arg(9)-bradykininen
dc.subjectportal hypertensionen
dc.subjectrat liver perfusionen
dc.titlePortal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B-2-type receptorsen
dc.typeinfo:eu-repo/semantics/article
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