【摘要】 目的　为探讨粥样硬化病变动脉对 5 - HT收缩反应增加的机制 ,观察与粥样硬化有关因子氧化低密度脂蛋白 (ox L DL)、低氧、5 - HT对血管平滑肌细胞 5 - HT2 A受体及其基因表达 ,以及细胞 [Ca2 + ]i的效应。方法　分别将大鼠主动脉平滑肌细胞单独以 5 0 μg/ m l ox L DL 培养 8h,2 %低氧处理 2 4和 48h,10 μm ol/ L 5 - HT处理30 min,放射配基结合分析测定 5 - HT2 A受体 ;RT- PCR和 Southern杂交检测受体基因的 m RNA;激光共聚焦扫描显微镜测单个细胞 [Ca2 + ]i。结果　经 ox L DL、低氧、 5 - HT处理 ,血管平滑肌细胞 5 - HT2 A受体显著上调 (P<0 .0 1) ;ox L DL及低氧处理的受体基因的 m RNA表达增加 ;ox L DL、低氧处理后 ,5 - HT刺激的血管平滑肌细胞[Ca2 + ]i升高幅度显著加大 (P<0 .0 5及 P<0 .0 1)。结论　 ox L DL、低氧、5 - HT引起血管平滑肌细胞 5 - HT2 A受体上调及细胞 [Ca2 + ]i增加 ,可能是粥样硬化动脉对 5 - HT收缩反应增强的部分原因。更多还原

【Abstract】 Objective To investigate the mechanisms of this hyperreactivity, the effects of oxLDL, hypoxia, and 5 HT (the relative factors inducing arteriosclerosis) on 5 HT 2A receptor, receptor gene expression and intracellular free Ca 2+ were observed in cultured rat aortic smooth muscle cells (ASMC). Methods ASMC underwent 50 μg/ml oxLDL 8 hours, 2% hypoxia 24 and 48 hours, 10 μmol/L 5 HT 30 min. 5 HT 2A receptor, 5 HT 2A receptor mRNA and [Ca 2+ ] i of ASMC were estimated by radiobinding assay, RT PCR and Southern blot method, and confocal laser scanning mode seperately. Results After oxLDL, hypoxia, 5 HT pretreatment, 5 HT 2A receptor of ASMC showed significant up regulation. Both 5 HT 2A receptor mRNA expression and 5 HT induced [Ca 2+ ] i of ASMC increased markedly after oxLDL, hypoxia pretreatment. Conclusions 5 HT 2A receptor up regulation and cell [Ca 2+ ] i increase of ASMC induced by oxLDL, hypoxia, and 5 HT may play a role in vascular hyperreactivity induced by 5 HT in atherosclerosis arteries.更多还原