Lipoxin A4 (LX4) is a biologically active product generated from arachidonic acid by lipoxygenase action and its formation is not inhibited by aspirin. In fact, aspirin triggers the production of lipoxins through acetylation of cyclooxygenase 2 (COX-2) that metabolizes arachidonic acid to 15(R)-hydroxyeicosatetraenoic acid. This metabolite is then converted, via lipoxygenase, to lipoxin, also known as “aspirin-triggered lipoxin”. LX4 has both anti-inflammatory and proinflammatory actions that are related with anaphylaxis, reocclusion and restenosis after coronary angioplasty in patients treated with aspirin. The formation of LX4 within the vascular lumen and wall during inflammation, e.g. after aspirin treatment, places this lipid in a strategically advantageous site for modulation of vascular function. However, little is known of the actions of LX4 on the vasculature. We hypothesized that LX4 would elicit contractile responses and will induce endothelial dysfunction in rat aorta. We used aorta from 12-week old male Wistar rats to assess vascular function on the pin myograph and reactive oxygen species (ROS) production via dihydroethidium fluorescence. LX4 (1-300 nM) induced concentration-dependent contractions and indomethacin, a COX inhibitor (INDO, 10 μM), did not affect this result (Emax, LX4: 30±6 vs. INDO: 20±1 % of KCl, p>0.05). Also, concentration-response curves to acetylcholine (ACh, 0.1 nM-30 μM) and phenylephrine (PE, 1 nM-30 μM) were performed in the absence (vehicle) or presence of LX4 (1 nM). LX4 increased aortic sensitivity to PE (pD2, vehicle: 7.37±0.05 vs. LX4: 7.64±0.07, p<0.05) and decreased ACh-induced relaxation (Emax, vehicle: 86±3 vs. LX4: 67±3 % of PE, p<0.05). Finally, incubation of aortic segments with LX4 (1 nM) for 15 min significantly increased dihydroethidium fluorescence (0.33±0.01 fold compared to vehicle, p<0.05), suggesting that LX4 may induce oxidative stress. In conclusion, these results show that LX4 has a functional role in aorta and may contribute to vascular dysfunction via increases in ROS. This lipid may contribute to further vascular damage in conditions where its production is exacerbated, such as in atherosclerosis or angioplasty-associated complications treated with aspirin.