EFFECT OF NIFEDIPINE ON INTRACELLULAR SIGNAL TRANSDUCTIONS IN HUMAN GINGIVAL FIBROBLASTS

人牙龈成纤维细胞是从接受钙通道阻滞剂药物治疗的患者中建立的，并通过前面描述的方法进行剩余牙齿的清除(Fujii等人，1994,1995)。经硝苯地平处理后，证实存在约30kD的特异性磷酸化蛋白。在缓激肽和/或硝苯地平治疗后，也观察到小蛋白的增加。IL-1和thapsigargin可增加细胞内碱性成纤维细胞生长因子，但不能增加硝苯地平的作用。经脱敏处理后，高亲和力碱性成纤维细胞生长因子结合部位减少了40%。硝苯地平可促进B受体激动剂异丙肾上腺素诱导的人牙龈成纤维细胞内cAMP的生成。在使用硝苯地平反应性患者牙龈成纤维细胞的实验中，提示硝苯地平反应性患者可能易受其他钙通道阻滞剂如尼卡地平、尼索地平、地尔硫卓、维拉帕米和苯妥英钠的影响。

Human gingival fibroblasts were established from the patients who had been receiving medication of calcium channel blockers, and undergone the clearance of remaining teeth by the method described previously (Fujii et al., 1994, 1995). After the treatment by nifedipine, the presence of specific phospholylated protein of approximately 30 Kd was confirmed. Increases of small proteins were also observed following the treatments by bradykinin and/or nifedipine. Interleukin-1 and thapsigargin increased intracellular bFGF, but not by nifedipine. The high affinity bFGF-binding site was decreased by 40% through desensitization process. The pre-treatment by nifedipine enhanced intracellular cAMP formation triggered by B-agonist, isoproterenol, in human gingival fibroblasts. In the experiment using gingival fibroblasts from nifedipine reactive patient, the possibility was suggested that nifedipine reactive patient might be susceptible to gingival overgrowth by other calcium channel blockers, such as nicardipine, nisoldipine, diltiazem, verapamil, and phenytoin.