Background: Angiotensin(Ang)-(1-7) is a biologically active member of the reninangiotensin
system that participates of the regulation of blood pressure. Although Ang-(1-7) is able
to potentiate the vasodilator effect of bradykinin in coronary bed of rats, a direct vasodilator effect
of Ang-(1-7) in this vascular bed has not been characterized.
Objectives: The aim of this study was to evaluate the mechanisms involved in the vasodilator effect
of Ang-(1-7) in the vasculature of isolated rat hearts perfused according to the Langendorff technique
at constant flow.
Methods: Isolated hearts, after approximately 30 minutes of stabilization, were perfused with
Krebs-Ringer solution (KRS) alone (control) or KRS containing Ang-(1-7). The participation of the
Ang-(1-7) receptor Mas, AT1 receptor, angiotensin-converting enzyme (ACE) and ACE2 was
evaluated perfusing hearts with a combination of Ang-(1-7) plus A779, Ang-(1-7) plus losartan,
Ang-(1-7) plus captopril/enalapril and Ang-(1-7) plus DX-600, respectively.
Results: Ang-(1-7) induced a significant decrease in the perfusion pressure, indicating a direct
vasodilatation action of this peptide in the coronary bed. This effect was abolished by A779, captopril,
enalapril and DX-600 an ACE2-specific inhibitor. However, AT1 blockade did not blunt the
Ang-(1-7) effect. No significant changes were observed in heart rate, as well as in contractile tension
and ±dT/dt. Moreover, immunohistochemical analysis showed the presence of Ang-(1-7) and
Mas in coronary vessels.
Conclusion: The Ang-(1-7) concentration used in this study was unable to induce changes in the
cardiac function since no consistent alterations in contraction force and HR were viewed after Ang-
(1-7) perfusion. In summary, this study showed that Ang-(1-7) induces vasodilation in the coronary
bed of rats and this effect involves coupling to Mas receptor and interaction with ACE and ACE2.