目的研究短期模拟失重条件下大鼠脑动脉血管平滑肌细胞(VSMCs)大电导钙激活钾通道(BKCa)与电压依赖性钾通道(KV)功能的改变。方法以尾部悬吊大鼠模型模拟失重对脑血管的影响,采用全细胞膜片钳记录模式,在细胞内液Ca2+保持生理浓度条件下,观察模拟失重1周后脑动脉VSMCs静息电位(RP)以及BKCa与KV电流密度的改变。结果与对照组相比,模拟失重1周后,RP更正,朝去极化方向改变;BKCa电流密度增大;但KV电流密度的变化则与检测电压有关,在-20～+20mV下,KV电流密度增大;而在+50～+60mV下,其电流密度减小。结论短期模拟失重已可引起脑动脉VSMCsBKCa与KV功能发生改变,既调节膜电位促进钙内流,又对其进行反馈调节防止血管紧张度过分增强,这可能是失重引起脑血管适应性变化的电生理机制之一。 Objective To study the changes of large-conductance calcium-activated-potassium channels (BKCa) and voltage-dependent potassium channels (KV) in rat cerebral arterial vascular smooth muscle cells (VSMCs) under short-term simulated weightlessness. Methods The rat model of tail suspension was used to simulate the effects of weightlessness on cerebrovascular. Using whole-cell patch-clamp recording mode, the resting potential (RP) of cerebral artery VSMCs after 1-week simulated weightlessness was observed under the condition of keeping the physiological concentration of Ca2 + Changes in BKCa and KV current densities. Results Compared with the control group, RP was corrected and depolarized in one week after simulated weightlessness, while the current density of BKCa increased. However, the change of KV current density was related to the detected voltage. Under -20 ~ + 20mV, KV Current density increases; while in the +50 ~ +60 mV, the current density decreases. Conclusions Short-term simulated weightlessness can cause changes in the functions of BKCa and KV in VSMCs, which not only regulate the membrane potential and promote calcium influx, but also prevent and control the excessive increase of vascular tone, which may be the impaired adaptive changes of cerebrovascular One of the physiological mechanisms.