Omega-6-derived lipid mediators are generally pro-inflammatory and have direct actions on the vascular wall (Félétou et al., 2010). By contrast, omega-3-derived fatty acids are well established to be cardioprotective (Kromhout & de Goede J, 2014), but the direct mechanism is unclear. Recently omega-3-derived metabolites, such as resolvins, have been shown to have key roles in the resolution of inflammation (Buckley et al., 2014) but the ability of these lipid mediators to act directly on vascular smooth muscle is unknown. The aim of the current project was to test whether resolvins D1, D2 and E1 have any vascular action.Segments of rat thoracic aorta were isolated and mounted on a wire myograph. Aorta segments were placed under a resting tension of 1.5 g and bathed in physiological saline solution (PSS) warmed to 37° C and continually gassed with 95% O2 and 5% CO2. Concentration-response curves were first constructed for phenylephrine (PE). Segments were then pre-constricted with a sub-maximal concentration of phenylephrine (EC80) and endothelial integrity was assessed with ACh (10 µM). Vessels were pre-constricted with PE again and vasodilatation to RvD1, RvD2 or RvE1 (0.1 µM) was assessed. Data are given as mean ± SEM and differences were assessed by one-way ANOVA with Bonferroni post hoc correction. Significance was accepted at p<0.05.As expected, PE produced concentration-dependent vasoconstriction, while ACh (10 µM) produced a profound vasodilatation in all segments (89.0 ± 4.1%, n=6, p<0.0001). None of the resolvins (0.1 µM) produced discernible relaxation of PE-induced constriction. The maximal relaxations to RvD1 (6.1 ± 6.5%; n=6), RvE1 (-3.4 ± 5.7%, n=6) and RvD2 (-0.3 ± 8.9%, n=6) were indistinguishable from time-matched controls.The proresolving lipid resolvins RvD1, RvD2 and RvE1 have no vasodilator effect on phenylephrine-constricted rat aorta segments, suggesting that they lack activity on vascular smooth muscle.