RESUMO
It has been shown that angiotensin-(1-7) (Ang-(1-7)) infusion potentiates the bradykinin (BK)-induced hypotensive response in conscious rats. The present study was conducted to identify Ang-(1-7)-BK interactions in the isolated rat heart perfused according to the Langendorff technique. Hearts were excised and perfused through the aortic stump under a constant flow with Krebs-Ringer solution and the changes in perfusion pressure and heart contractile force were recorded. Bolus injections of BK (2.5, 5, 10 and 20 ng) produced a dose-dependent hypotensive effect. Ang-(1-7) added to the perfusion solution (2 ng/ml) did not change the perfusion pressure or the contractile force but doubled the hypotensive effect of the lower doses of BK. The BK-potentiating Ang-(1-7) activity was blocked by pretreatment with indomethacin (5 mg/kg, ip) or L-NAME (30 mg/kg, ip). The Ang-(1-7) antagonist A-779 (50 ng/ml in Krebs-Ringer) completely blocked the effect of Ang-(1-7) on BK-induced vasodilation. These data suggest that the potentiation of the BK-induced vasodilation by Ang-(1-7) can be attributed to the release of nitric oxide and vasodilator prostaglandins through an Ang-(1-7) receptor-mediated mechanism.
Assuntos
Angiotensina I/farmacologia , Bradicinina/farmacologia , Vasos Coronários/efeitos dos fármacos , Fragmentos de Peptídeos/farmacologia , Vasodilatadores/farmacologia , Análise de Variância , Animais , Fármacos Cardiovasculares/farmacologia , Sinergismo Farmacológico , Inibidores Enzimáticos/farmacologia , Indometacina/farmacologia , Masculino , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico/fisiologia , Ratos , Ratos WistarRESUMO
It has been shown that angiotensin-(1-7) (Ang-(1-7)) infusion potentiates the bradykinin (BK)-induced hypotensive response in conscious rats. The present study was conducted to identify Ang-(1-7)-BK interactions in the isolated rat heart perfused according to the Langendorff technique. Hearts were excised and perfused through the aortic stump under a constant flow with Krebs-Ringer solution and the changes in perfusion pressure and heart contractile force were recorded. Bolus injections of BK (2.5, 5, 10 and 20 ng) produced a dose-dependent hypotensive effect. Ang-(1-7) added to the perfusion solution (2 ng/ml) did not change the perfusion pressure or the contractile force but doubled the hypotensive effect of the lower doses of BK. The BK-potentiating Ang-(1-7) activity was blocked by pretreatment with indomethacin (5 mg/kg, ip) or L-NAME (30 mg/kg, ip). The Ang-(1-7) antagonist A-779 (50 ng/ml in Krebs-Ringer) completely blocked the effect of Ang-(1-7) on BK-induced vasodilation. These data suggest that the potentiation of the BK-induced vasodilation by Ang-(1-7) can be attributed to the release of nitric oxide and vasodilator prostaglandins through an Ang-(1-7) receptor-mediated mechanism.
Assuntos
Animais , Masculino , Ratos , Angiotensina I/farmacologia , Bradicinina/farmacologia , Vasos Coronários/efeitos dos fármacos , Vasodilatadores/farmacologia , Análise de Variância , Fármacos Cardiovasculares/farmacologia , Inibidores Enzimáticos/farmacologia , Hipotensão , Indometacina/farmacologia , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico , Ratos WistarAssuntos
Aneurisma Coronário/diagnóstico por imagem , Síndrome de Linfonodos Mucocutâneos/complicações , Aspirina/uso terapêutico , Aneurisma Coronário/etiologia , Dipiridamol/uso terapêutico , Ecocardiografia , Feminino , Humanos , Lactente , Síndrome de Linfonodos Mucocutâneos/tratamento farmacológicoRESUMO
Os autores estudam 10 casos de cisto popliteo na artrite reumatoide com comunicacao para a articulacao femorotibial tratados pela sinovectomia anterior do joelho e enfatizam que o cisto popliteo, sendo apenas o resultado da alta pressao intraarticular produzida pelos fenomenos inflamatorios da artrite reumatoide, devera ser tratado pela sinovectomia do joelho comprometido e nao pela resseccao do cisto comunicante