Key points Two distinct angiotensin‐(1–7) [Ang‐(1–7)] receptor blockers, A779 and d‐Pro‐Ang‐(1–7), can completely prevent Ang‐(1–7)‐induced vasorelaxation. Genetic deficiency of Mas completely prevents vascular responses to Ang‐(1–7). Genetic deficiency of Mas completely prevents vascular responses to other NO‐dependent vasorelaxants (bradykinin). Mas plays a key role in NO‐mediated vasodilatation by modulating vasorelaxant‐mediated phosphorylation of endothelial nitric oxide synthase in endothelial cells. Abstract  The heptapeptide angiotensin‐(1–7) is a biologically active metabolite of angiotensin II, the predominant peptide of the renin–angiotensin system. Recently, we have shown that the receptor Mas is associated with angiotensin‐(1–7)‐induced signalling and mediates, at least in part, the vasodilatory properties of angiotensin‐(1–7). However, it remained controversial whether an additional receptor could account for angiotensin‐(1–7)‐induced vasorelaxation. Here, we used two different angiotensin‐(1–7) antagonists, A779 and d‐Pro‐angiotensin‐(1–7), to address this question and also to study their influence on the vasodilatation induced by bradykinin. Isolated mesenteric microvessels from both wild‐type and Mas‐deficient C57Bl/6 mice were precontracted with noradrenaline, and vascular reactivity to angiotensin‐(1–7) and bradykinin was subsequently studied using a small‐vessel myograph. Furthermore, mechanisms for Mas effects were investigated in primary human umbilical vein endothelial cells. Both angiotensin‐(1–7) and bradykinin triggered a concentration‐dependent vasodilatation in wild‐type microvessels, which was absent in the presence of a nitric oxide synthase inhibitor. In these vessels, the pre‐incubation with the Mas antagonists A779 or d‐Pro‐angiotensin‐(1–7) totally abolished the vasodilatory capacity of both angiotensin‐(1–7) and bradykinin, which was nitric oxide mediated. Accordingly, Mas‐deficient microvessels lacked the capacity to relax in response to either angiotensin‐(1–7) or bradykinin. Pre‐incubation of human umbilical vein endothelial cells with A779 prevented bradykinin‐mediated NO generation and NO synthase phosphorylation at serine 1177. The angiotensin‐(1–7) antagonists A779 and d‐Pro‐angiotensin‐(1–7) equally block Mas, which completely controls the angiotensin‐(1–7)‐induced vasodilatation in mesenteric microvessels. Importantly, Mas also appears to be a critical player in NO‐mediated vasodilatation induced by renin–angiotensin system‐independent agonists by altering phosphorylation of NO synthase.