Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart

• Main Authors: A.P. Almeida, B.C. Frábregas, M.M. Madureira, R.J.S. Santos, M.J. Campagnole-Santos, R.A.S. Santos
• Format: Article
• Language: English
• Published: Associação Brasileira de Divulgação Científica 2000-06-01
• Series: Brazilian Journal of Medical and Biological Research
• Subjects: angiotensin-(1-7); bradykinin; coronary artery; rat heart; L-NAME; prostaglandins; bradykinin potentiation
• Online Access: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000000600012
• ISSN: 0100-879X; 1414-431X

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.