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

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

Autor Gioli-Pereira, L. Google Scholar
Nascimento, E. A. Google Scholar
Santos, E. L. Google Scholar
Bracht, A. Google Scholar
Juliano, M. A. Google Scholar
Pesquero, J. B. Google Scholar
Borges, D. R. Google Scholar
Kouyoumdjian, M. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Maringa State Univ
Resumo Background 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.
Palavra-chave angiotensin converting enzyme
bradykinin receptor
hepatic microcirculation
portal hypertension
sinusoidal liver cells
Idioma Inglês
Data de publicação 2005-03-01
Publicado em Journal of Gastroenterology and Hepatology. Carlton: Blackwell Publishing Asia, v. 20, n. 3, p. 463-473, 2005.
ISSN 0815-9319 (Sherpa/Romeo, fator de impacto)
Publicador Blackwell Publishing Asia
Extensão 463-473
Fonte http://dx.doi.org/10.1111/j.1440-1746.2005.03580.x
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000227948100021
Endereço permanente http://repositorio.unifesp.br/handle/11600/28189

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