Angiotensin-(1–7) Augments Bradykinin-Induced Vasodilation by Competing With ACE and Releasing Nitric Oxide

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Abstract
Recent studies have shown that angiotensin-(1–7) [Ang-(1–7)] interacts with kinins and augments bradykinin (BK)-induced vasodilator responses by an unknown mechanism. In this study, we evaluated whether the potentiation of the BK-induced vasodilation by Ang-(1–7) may be attributable to inhibition of BK metabolism, release of nitric oxide, or both. Isometric tension was measured in intact canine coronary artery rings suspended in organ chambers. 125I-[Tyr0]-BK metabolism was determined in vascular rings by assessing the degradation of the peptide by high-performance liquid chromatography. Ang-(1–7) augmented the vasodilation induced by BK in a concentration-dependent manner in rings preconstricted with the thromboxane analog U46619. The EC50 of BK (2.45±0.51 nmol/L versus 0.37±0.08 nmol/L) was shifted leftward by 6.6-fold in the presence of 2 μmol/L concentration of Ang-(1–7). The response was specific for BK, since Ang-(1–7) did not augment the vasodilation induced by either acetylcholine (0.05 μmol/L) or...