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失调的一个重要因素，其发生机理目前仍不甚清楚，也缺乏有效的对抗措施。L型电压依赖性钙通道(CaL）在血管平滑肌细胞（VSMCs）上广泛分布，对血管的功能与结构起着重要的调控作用。我们前期工作已证实模拟失重可引起大鼠脑动脉收缩功能增强、结构发生肥厚性重建，且脑动脉VSMCs膜上CaL通道功能在白天(12 h光照)与夜间（12 h黑暗）时均显著增强，提示CaL通道昼夜节律的改变可能参与模拟失重大鼠脑动脉功能与结构的重建过程，但其作用机理却不清楚。本项目拟采用电生理膜片钳、分子生物学方法、血管体外培养与细胞转染等技术从动物整体、器官、细胞与基因等多个水平探讨CaL通道昼夜节律的改变机理及其在模拟失重大鼠脑动脉重建中的作用。本项目可对航天失重环境下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. L-type voltage-dependent calcium (CaL) channels are highly expressed in vascular smooth muscle cells (VSMCs). It is believed that CaL channels play an essential role in the regulation of vascular function and structure. Our previous work has reported that simulated microgravity induced enhanced contraction and hypertrophic adaptation in rat cerebral arteries. Furthermore, we also demonstrated that simulated microgravity increased the function of CaL channel not only in daytime (12 h light) but also in nighttime (12 h dark) as compared with the control. These results suggested that the circadian regulation of CaL channels has changed in cerebral arterial remodeling of simulated microgravity rats. However, the precise mechanisms remain to be determined. In the present study, we want to investigate the role of circadian regulation of CaL channels in simulated microgravity rats with electrophysiology, molecular biology, culture cell, and cell transformation techniques in vivo and in vitro. Our study may provide a novel mechanism for cerebrovascular remodeling during real/simulated microgravity. We also want to find the zeitgeber medicine for contermeasures to ensure the health and efficiency for astronauts.