recovery and conversion of kinins by exsanguinated rat preparations

Prado, J. L.; Limãos, E. A.; Roblero, J.; Freitas, J.O.; Prado, Eline S.; Paiva, A. C. M.

doi:10.1016/0024-3205(75)90399-9

Cited by 2 publications

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“…The cleavage of Lys-BK by aminopeptidase generates BK, and cleavage by carboxypeptidase generates des-Arg 9 -BK and des-Arg 9 Lys-BK. Several enzymes are responsible for inactivation and metabolism of BK; for a long period of time, inactivation was attributed almost exclusively to angiotensinconverting enzyme (ACE) from the lung, although the liver plays an important role in BK inactivation (Prado et al 1975). Hepatic modulation of KS, as demonstrated by the isolated and exanguinated perfused rat liver model, is shown in Figure 1.…”

Section: Characteristics Of the Kinin System And Its Role In Diseasesmentioning

confidence: 99%

Portal hypertensive response to kinin

Kouyoumdjian

Nagaoka

Loureiro-Silva

et al. 2009

An. Acad. Bras. Ciênc.

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Portal hypertension is the most common complication of chronic liver diseases, such as cirrhosis. The increased intrahepatic vascular resistance seen in hepatic disease is due to changes in cellular architecture and active contraction of stellate cells. In this article, we review the historical aspects of the kallikrein-kinin system, the role of bradykinin in the development of disease, and our main findings regarding the role of this nonapeptide in normal and experimental models of hepatic injury using the isolated rat liver perfusion model (mono and bivascular) and isolated liver cells. We demonstrated that: 1) the increase in intrahepatic vascular resistance induced by bradykinin is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and is preserved in the presence of inflammation, fibrosis, and cirrhosis; 2) the hepatic arterial hypertensive response to bradykinin is calcium-independent and mediated by eicosanoids; 3) bradykinin does not have vasodilating effect on the pre-constricted perfused rat liver; and, 4) after exertion of its hypertensive effect, bradykinin is degraded by angiotensin converting enzyme. In conclusion, the hypertensive response to BK is mediated by the B2 receptor in normal and pathological situations. The B1 receptor is expressed more strongly in regenerating and cirrhotic livers, and its role is currently under investigation.

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Section: Characteristics Of the Kinin System And Its Role In Diseasesmentioning

confidence: 99%

Portal hypertensive response to kinin

Kouyoumdjian

Nagaoka

Loureiro-Silva

et al. 2009

An. Acad. Bras. Ciênc.

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show abstract

“…A inativação fisiológica da bradicinina (BK) foi, durante algum tempo, atribuída quase exclusivamente à ação da cininase II (enzima conversora de angiotensina, ACE) encontrada no endotélio vascular, principalmente na circulação pulmonar. Entretanto, o fígado também apresenta importante atividade cininásica 3,4 . Recentemente, demonstramos 5 a semelhança entre a endopeptidase hepática inativadora de bradicinina (principal cininase hepática) e a metaloendopeptidas etiol-dependente EC 3.4.24.15.…”

Section: Introductionunclassified