Nitric oxide released from vascular endothelium plays important regulatory roles in cardiovascular and pulmonary systems. Epidemiological studies suggest that diesel exhaust particles (DEP) seem to be one of the causative factors responsible for the recent increase in pulmonary diseases. To clarify the pathogenic mechanism, the effects of DEP on vascular endothelial functions were investigated in terms of endothelium-dependent relaxation. Ring preparations of rat thoracic aorta were preincubated for 10 min with a DEP suspension (1, 10, 100 μg/ml) at 37°C in organ baths and relaxed with cumulative additions of acetylcholine following precontraction with phenylephrine (10^-6 M). The relaxation was attenuated by DEP-exposure in a concentration-dependent manner. An addition of superoxide dismutase (SOD) completely abolished the inhibitory effect of DEP at lower concentrations, but only partially at the higher concentration. DEP (10 μg/ml) neither affected the contractile response to phenylephrine in intact aortic rings nor the endothelium-independent relaxation by sodium nitroprusside in denuded rings, while DEP (100 μg/ml) significantly attenuated both responses. These results suggest that 1) inhaled DEP causes pulmonary inflammation by inhibiting the endothelial formation and/or the effect of nitric oxide and 2) SOD reduces the adverse effects.