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目的 探讨钙超载模型大鼠血管平滑肌细胞 (VSMC)胞内是否存在钙离子 (Ca2 + )稳态调节异常。方法 以 Fluo- 3/AM作为 Ca2 + 指示剂 ,应用激光扫描共聚焦显微镜技术 ,比较钙超载模型大鼠肠系膜 VSMC(Ca OMV)与正常 Wistar大鼠肠系膜 VSMC(WMV )静息态的胞浆与核内游离 Ca2 + 水平 ([Ca2 + ]i,[Ca2 + ]n) ,以及在多种药物刺激下 Ca2 +稳态调节的差异。结果 两种 VSMC静息态 [Ca2 + ]i及 [Ca2 + ]n 并无显著性差异 ,但在KCl、Bay- k86 44、Ang- 、IP3、CHCl3和 CPA等药物作用下 ,Ca OMV [Ca2 + ]i与 [Ca2 + ]n的升高幅度较 WMV显著增大 (P<0 .0 1)。结论 (1) Ca OMV对激动剂作用的敏感性增强 ,存在 Ca2 + 稳态调节异常 ,提示胞内钙超载与胞外钙超载同时共存 ,是血管硬化和老化机制的两个方面 ;(2 )血管钙超载时 ,VSMC无论质膜上的 Ca2 + 门控系统还是胞内钙池的释放与重储均有异常 ;(3)在 Ca OMV,胞浆与核内钙的调节均存在异常。
Objective To investigate whether there is Ca (2+) homeostasis in the vascular smooth muscle cells (VSMC) of rats with calcium overload. Methods Fluo-3 / AM was used as a Ca2 + indicator. Laser scanning confocal microscopy was used to compare the resting cytoplasm of mesentery VSMC (WMV) between mesentery VSMC (Ca OMV) and normal Wistar rats Intracellular free Ca2 + levels ([Ca2 +] i, [Ca2 +] n), and differences in Ca2 + homeostasis under various drug-stimuli. Results There was no significant difference in the resting state [Ca2 +] i and [Ca2 +] n between the two VSMCs. However, under the action of KCl, Bay- k86 44, Ang-, IP3, CHCl3 and CPA, +] i and [Ca2 +] n increased significantly more than WMV (P <0.01). Conclusions (1) The sensitivity of Ca OMV to agonist action is enhanced, and there is abnormal regulation of Ca2 + homeostasis, suggesting that intracellular Ca2 + overload coexists with extracellular Ca2 + overload, which are two aspects of vascular sclerosis and aging mechanism. (2) Vascular calcium overload, VSMC regardless of the plasma membrane Ca2 + gating system or intracellular calcium release and re-storage are abnormal; (3) in Ca OMV, the regulation of cytoplasm and nuclear calcium are abnormal.