Reversible photorelaxations elicited by ultraviolet light (UV, 366 nm) of the isolated longitudinal strips of mouse gastric fundus precontracted with 1 mu M methacholine (MCh) were significantly enhanced by either sodium nitrite (NaNO2, 10 mu M-1 mM) or N-omega-nitro-L-arginine (L-NOARG, 1-100 mu M), in concentration-dependent manner. Acidified NaNO2 but not neutral NaNO2 and L-NOARG produced relaxation similar to the photorelaxation. Hemoglobin (Hb, 1-50 mu M), hydroxocobalamine (Hc, 30 and 50 mu M) and ferrous sulfate (FeSO4, 10 mu M -1 mM) inhibited the photorelaxation observed in the absence or presence of NaNO2 or L-NOARG (both 100 mu M) Similar effects were also observed with the acidified NaNO2 induced relaxations. Methylene blue (Mb, 10 and 50 mu M) did not affect photorelaxations potentiated by NaNO2 and L-NOARG but inhibited photorelaxations induced by UV light alone. Superoxide dismutase (SOD, 15-100 mu M) enhanced both relaxations induced by UV light and potentiatiation by photoactivated nitro compounds. Sodium nitroprusside (SNP, 0.1-10 mu M) also potentiated photorelaxations. On the other hand, neither L-arginine (L-ARG, 500 mu M and 1 mM) nor N-G-methyl-L-arginine (L-NMMA, 10 mu M) was found to be effective on photorelaxations produced by UV light alone. 0.5 mu M tetrodotoxin (TTX) did not inhibit relaxation induced by photoactivated NaNO2 (100 mu M), a finding eliminating the involvement of a neuronal component. These results support the notion that the release of nitric oxide (NO) may be essential for smooth muscle relaxation by UV light in isolated mouse gastric fundus.