Acrolein is a highly reactive aldehyde pollutant and an endogenous product of lipid peroxidation. Increased generation of, or exposures to, acrolein incites pulmonary and vascular injury. To understand its mechanism of action, the effects of acrolein on the vasomotor responses of rat aortic rings were studied. Incubation with acrolein (10-100 µM) alone did not affect the resting tone of aortic vessels, however, a dose-dependent relaxation of phenylephrine pre-contracted aortic rings was observed. Acrolein-induced relaxation was slow and time-dependent and the extent of relaxation after 100 min of application was: 44.7 ± 4.1 % (10 µM), 56.0 ± 5.6 % (20 µM), 61.0 ± 7.9 % (40 µM) and 96.1 ± 2.1 % (80 µM) respectively, vs. 14.2 ± 3.3 % relaxation in the absence of acrolein. Acrolein-induced vasorelaxation was prevented by endothelial denudation and was abolished upon pretreatment with the nitric oxide synthase inhibitor - N-nitro-L-arginine-methyl ester, guanylyl cyclase inhibitor - 1H-[1,2,4,]oxidazolo-[4,3-a] quinoxalin-1-one, or the cyclooxygenase inhibitor - indomethacin. Inhibition of K+ channels (by tetrabutylammonium) or Na⁺, K⁺- ATPase (by ouabain) did not significantly prevent acrolein-mediated vasorelaxation. Exposure to acrolein in the presence or absence of other compounds elicited slow wave vasomotor effect in 77 % of aortic vessels vs. 1.4 % in control. Vasomotor responses were also studied on aortic rings prepared from rats fed 2 mg/kg/day acrolein for 3 alternate days by oral gavage. These vessels developed a significantly lower contractile response to phenylephrine as compared to controls. Together, these results indicate that acute acrolein exposure evokes delayed vasorelaxation due to a NO- and prostacyclin-dependent mechanism, while in vivo acrolein exposure compromises vessel contractility.