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Interação angiotensina-(1-7) e bradicinina na microcirculação mesentérica, in vivo in situ. / Synergistic effect of angiotensin-(1-7) on bradykinin arteriolar dilation in vivo.

Interação entre angiotensina-(1-7) [Ang-(1-7)] e bradicinina (BK) foi determinada no mesentério de ratos Wistar anestesiados utilizando-se microscopia intravital. Aplicação tópica de BK e Ang-(1-7) induziram vasodilatação que foi abolida por HOE-140 e A-779, respectivamente. Ang-(1-7) (100 pmol) potencializou a vasodilatação de BK (1 pmol) mas não a vasodilatação promovida por acetilcolina, nitroprussiato de sódio, histamina e ácido araquidônico. O efeito potencializador de Ang-(1-7) sobre BK foi abolido por A-779, HOE-140, indometacina, L-NAME e TEA, entretanto, losartan não bloqueou este efeito. Enalaprilato aumentou a resposta vasodilatadora de BK e Ang-(1-7) e não alterou o efeito potencializador do segundo sobre o primeiro. Conclui-se que: 1)efeito potencializador de Ang-(1-7) sobre BK depende da interação de ambos com seus respectivos receptores; 2)é dependente de óxido nítrico, produtos da cicloxigenase e hiperpolarização de membrana via canais de potássio; 3) o mecanismo de potencialização parece não depender da atividade catalítica da ECA. / The interaction between angiotensin-(1-7) [Ang-(1-7)] and bradykinin (BK) was determined in the mesentery of anesthetized Wistar rats using intravital microscopy. The response-induced by topical application of BK (1, 10 and 30 pmol), Ang-(1-7) (1, 10, 100 and 1000 pmol) and Ang-(1-7) (100 pmol) + BK (1 pmol) was determined in mesenteric arterioles (15-20 mm diameter). The BK (1 pmol)- and Ang-(1-7) (100 pmol)- induced vasodilation was abolished by BK B2 receptor antagonist HOE-140 (100 pmol applied during 60 seconds) and the Ang-(1-7) antagonist [d-Ala7]-Ang-(1-7)] (A-779) (100 pmol applied during 15 seconds), respectively. Indomethacin (5 mg/kg; IM, 30 min before), a cyclooxygenase inhibitor; L-NAME (10 nmol; topical application, 3 min before), a NO synthase inhibitor, decreased the Ang-(1-7)-induced vasodilation. However, TEA (90 pmol; topical application), a non specific K+ channels blocker, did not alter the response to BK or Ang-(1-7). BK (1 pmol)-induced vasodilation, however, was potentiated by Ang-(1-7) 100 pmol. Sodium nitroprusside (38 pmol), acetylcholine (1,6 nmol), histamine (5,4 nmol) and arachdonic acid (10 nmol) responses were not modified by Ang-(1-7) 100 pmol. The Ang-(1-7)-potentiating effect on BK-induced vasodilation was abolished by A-779, HOE-140, indomethacin, L-NAME and TEA. Losartan (15 mg/kg.IV, 40 min before), an AT1 angiotensin receptor antagonist was without effect. On the other hand, enalaprilat treatment (10 mg/kg; IV, 30 min before), to inhibit angiotensin-converting enzyme (ACE), enhanced the BK and Ang-(1-7)-induced vasodilation but did not modify the effect of Ang-(1-7) on BK vasodilation. In conclusion, the potentiation of BK-induced vasodilation by Ang-(1-7) is a receptor-mediated phenomenon dependent on cyclooxygenase-related products, NO release and K+ channel-mediated membrane hyperpolarization. The potentiating mechanism, apparently, is not related to ACE catalytic activity.

Identiferoai:union.ndltd.org:IBICT/oai:teses.usp.br:tde-22032001-163029
Date11 July 2000
CreatorsMaria Aparecida de Oliveira
ContributorsZuleica Bruno Fortes, Debora Rejane Fior Chadi, Jose Eduardo Krieger
PublisherUniversidade de São Paulo, Farmacologia, USP, BR
Source SetsIBICT Brazilian ETDs
LanguagePortuguese
Detected LanguageEnglish
Typeinfo:eu-repo/semantics/publishedVersion, info:eu-repo/semantics/masterThesis
Sourcereponame:Biblioteca Digital de Teses e Dissertações da USP, instname:Universidade de São Paulo, instacron:USP
Rightsinfo:eu-repo/semantics/openAccess

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