We examined a participation of photochemical nitric oxide in the vasorelaxation induced by ultraviolet pulsed light. We measured a luminal diameter of rat femoral artery in vivo during a Krypton-fluoride (KrF) excimer laser irradiation. We also measured the vascular response when the artery was pretreated with sodium nitrite, superoxide dismutase or methylene blue. Histological changes in the vessels were examined by light microscopy. The vessel relaxed by KrF laser. The vasorelaxation was dependent on the repetition rate under the constant total energy. On the contrary, the vessel wall damage was inversely proportional to the repetition rate. Accordingly, the damage is most likely due to photoacoustic mechanism. The vasorelaxation was inhibited by methylene blue but enhanced by sodium nitrite or superoxide dismutase, which strongly suggests that the relaxation is closely related to nitric oxide. We conclude that the photochemical product of nitric oxide may be one of the possible mechanisms for the pulsed ultraviolet light induced vasorelaxation.