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

Brazilian Journal of Medical and Biological Research

A.p. Almeida¹  B.c. Frábregas¹  M.m. Madureira¹  R.j.s. Santos¹  M.j. Campagnole-santos¹  R.a.s. Santos¹ 

[1] ,Universidade Federal de Minas GeraisBelo Horizonte MG ,Brasil

关键词: angiotensin-(1-7);    bradykinin;    coronary artery;    rat heart;    L-NAME;    prostaglandins;    bradykinin potentiation;   

DOI  :  10.1590/S0100-879X2000000600012

来源: SciELO

【 摘 要 】

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.

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