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Objective: The involvement of purinergic signaling in the modulation of vascular dysfunction is an emerging field of research. The aim of the present study was to investigate the role of the purinergic receptor P2Y11 in the modification of vascular reactivity and reactive oxygen species (ROS) production induced by angiotensin II (Ang II) stimulation. Materials and Methods: To this aim, rat aortic rings were incubated with Ang II (100 nM, 30 min) in the presence vs. absence of the P2Y11 receptor activator (NF546, 10 μmol/L) with or without the P2Y11 inhibitor (NF340, 10 μmol/L). Aortic rings were used for vasomotor studies (DMT myograph) and the assessment of hydrogen peroxide (H2O2) production by means of Ferrous iron xylenol orange OXidation (FOX assay). Results: Activation of P2Y11 receptor with NF546 reduced the contractility to phenylephrine, improved the endothelial-dependent relaxation to acethylcholine, reduced contractility to L-NAME, and decreased H2O2 production in aortic rings exposed to Ang II. These effects were blocked in the presence of the P2Y11 receptor inhibitor (NF340). Conclusion: Activation of P2Y11 purinergic receptor alleviated endothelial dysfunction and mitigated oxidative stress elicited by acute ex vivo exposure to Ang II. Further investigations are required in order to elucidate the signal transduction mechanisms of the purinergic-mediated vasculoprotection. [ABSTRACT FROM AUTHOR]