To clarify the mechanism of the contractile responses induced by ultraviolet light radiation (UVR-contraction) in the intact endothelial rings of rat isolated thoracic aortae precontracted with 10-6M phenylephrine, effects of various calcium channel blockers and Bay K 8644 were investigated. The doses of calcium channel blockers which inhibited 50mM KCl-induced contraction less than 30% were used in this experiment. Phenylephrine-induced contractions (PE-contraction) were inhibited markedly by diltiazem (DT), verapamil (VP), nifedipine (NF), and MgSO4, while flunarizine (FN) and nimodipine (NM) transiently potentiated PE-contraction, then significantly inhibited the contraction. Though UVR-contraction was significantly potentiated by 10(-6)M DT, NF, NM, and 10(-7)M FN, the contraction markedly attenuated by 10(-7)M NF and 1mM MgSO4. However, 10(-5)M DT, 10(-6) and 10(-5)M VP, 10(-6)M FN, 10(-7)M NM, 10(-7) and 10(-6)M nicardipine did not affect UVR-contraction. These multiform effects of calcium channel blockers suggest that the blockers do not affect UVR-contraction in uniform fashion. In both preparations with and without endothelium, 10(-6)M Bay K 8644 markedly potentiated PE-contraction. After treatment with Bay K 8644, UVR-contraction was reversed in rings without endothelium was significantly potentiated. In conclusion, the above results suggest that the mechanism involved in UVR-contraction is different from the mechanism of contractile response to KCl and/or to PE.