Fate of bradykinin on the rat liver when administered by the venous or arterial route

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dc.contributor.authorGioli-Pereira, L.
dc.contributor.authorNascimento, E. A.
dc.contributor.authorSantos, E. L.
dc.contributor.authorBracht, A.
dc.contributor.authorJuliano, M. A.
dc.contributor.authorPesquero, J. B.
dc.contributor.authorBorges, D. R.
dc.contributor.authorKouyoumdjian, M.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionMaringa State Univ
dc.date.accessioned2016-01-24T12:37:43Z
dc.date.available2016-01-24T12:37:43Z
dc.date.issued2005-03-01
dc.description.abstractBackground and Aim: Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver.Method: BK, HOE-140 (a B2R antagonist), des-R-9-BK (a BIR agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays.Results: Des-R-9-BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium-dependent PHR and a calcium-independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R-1-F-5 and R-1-P-7) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist.Conclusions: Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes. (C) 2005 Blackwell Publishing Asia Pty Ltd.en
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.affiliationUniversidade Federal de São Paulo, Dept Med, São Paulo, Brazil
dc.description.affiliationMaringa State Univ, Dept Biochem, Parana, 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.affiliationUnifespUniversidade Federal de São Paulo, Dept Med, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent463-473
dc.identifierhttp://dx.doi.org/10.1111/j.1440-1746.2005.03580.x
dc.identifier.citationJournal of Gastroenterology and Hepatology. Carlton: Blackwell Publishing Asia, v. 20, n. 3, p. 463-473, 2005.
dc.identifier.doi10.1111/j.1440-1746.2005.03580.x
dc.identifier.issn0815-9319
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28189
dc.identifier.wosWOS:000227948100021
dc.language.isoeng
dc.publisherBlackwell Publishing Asia
dc.relation.ispartofJournal of Gastroenterology and Hepatology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectangiotensin converting enzymeen
dc.subjectbradykinin receptoren
dc.subjecthepatic microcirculationen
dc.subjectportal hypertensionen
dc.subjectsinusoidal liver cellsen
dc.titleFate of bradykinin on the rat liver when administered by the venous or arterial routeen
dc.typeinfo:eu-repo/semantics/article
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