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Titolo:
Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B-2-type receptors
Autore:
Loureiro-Silva, MR; Molina, HM; Borges, DR;
Indirizzi:
Univ Fed Sao Paulo, Lab Expt Hepatol Nucleo Metab Hepat, Sao Paulo, BrazilUniv Fed Sao Paulo Sao Paulo Brazil cleo Metab Hepat, Sao Paulo, Brazil
Titolo Testata:
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
fascicolo: 1, volume: 16, anno: 2001,
pagine: 41 - 45
SICI:
0815-9319(200101)16:1<41:PHRTBI>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; PLASMA KALLIKREIN; KININ B-1; CLEARANCE;
Keywords:
acute phase response; bradykinin antagonist; bradykinin receptor; bradykinin; cirrhosis; des-Arg(9)-bradykinin; portal hypertension; rat liver perfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Borges, DR Rua Jabuticabeiras 807, BR-05674011 Sao Paulo, Brazil Rua Jabuticabeiras 807 Sao Paulo Brazil BR-05674011 BC Brazil
Citazione:
M.R. Loureiro-Silva et al., "Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B-2-type receptors", J GASTR HEP, 16(1), 2001, pp. 41-45

Abstract

Background: 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 doseof 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 orcirrhotic 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:41:30