航天失重环境所引起的脑动脉功能与结构重建是航天员“心脑血管功能失调”的重要因素，其发生机理目前仍不甚清楚，也缺乏有效对抗措施。我们前期工作证实模拟失重可引起大鼠脑动脉血管平滑肌细胞（VSMCs）线粒体膜电位与活性氧含量在白天（12 h光照）与夜间（12 h黑暗）均发生改变且昼夜振荡幅度明显降低，而线粒体内膜上的大电导钙激活钾通道（mitoBKCa）可参与这一变化过程，其机制可能涉及时钟基因Bmal1的转录调控与长链非编码RNA（LncRNA）的变化。本项目拟采用电生理膜片钳、分子生物学方法、血管体外培养、细胞转染与基因敲除小鼠等技术从动物整体、器官、细胞与基因等多个水平探讨mitoBKCa通道在模拟失重大鼠脑动脉VSMCs线粒体似昼夜节律紊乱及脑动脉重建过程中的作用。本项目可对航天失重环境脑动脉的重建机制提出新的思路，并希望找到受时因子药物作为预防与对抗措施，以保证航天员的健康与工作效率。

Cerebrovascular remodeling has been regarded as one of important factors which may induce postspaceflight cardiovascular dysfunction. However, the mechanism remains unknown and there are still no effective countermeasures. Our previous work has demonstrated that simulated microgravity disrupted the circadian rhythm in the mitochondrial membrane potential and reactive oxygen species (ROS）by decreasing the oscillating amplitude between light-time (12 h) and dark-time (12 h). We also found that mitochondrial large conductance Ca2+ activated-K+ channels participate in the mitochondrial circadian and the related signal pathway may include the clock gene, Bmal1 and the Long non-coding RNA (LncRNA). In the present study, we want to investigate the role of circadian regulation of mitoBKCa channels in cerebral vascular smooth muscle cells of simulated microgravity rats with electrophysiology, molecular biology, culture cell, transformation, and knock-out mice. Our study may provide a novel mechanism for cerebrovascular remodeling during real/simulated microgravity. We also want to find the zeitgeber medicine for countermeasures to ensure the health and efficiency for astronauts.