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Chonnam Med J. 1999 Sep;35(3):387-398. Korean. Original Article.
Yoon KM , Kim KS , Kim DY , Lee SY , Cho BH , Baik YH .
Department of Plastic reconstructive surgery, Chonnam university Medical school, Kawngju, Korea.
Department of Pharmacology, Chonnam university Medical school, Kawngju, Korea.

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.

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