已有研究表明模拟失重可引起大鼠脑动脉发生区域特异性变化,其中Ca2+通道和肾素-血管紧张素系统(renin-angio-tensin system,RAS)可能发挥着重要的作用。本研究旨在探讨血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)对短期模拟失重大鼠脑基底动脉血管平滑肌细胞(vascular smooth muscle cells,VSMCs)L-型Ca2+通道(L-type calcium channel,CaL)功能的影响。模拟失重(尾部悬吊)3d后,用木瓜蛋白酶法分离大鼠脑基底动脉VSMCs。采用全细胞膜片钳技术,以Ba2+作为载流子,测定CaL电流密度,然后观察Ang Ⅱ对该电流的影响。结果显示,模拟失重3d对大鼠脑基底动脉VSMCs的膜电容和接入电阻无明显影响,但可致VSMCs的CaL电流密度显著增加。不过,模拟失重对CaL的电压激活特性和稳态激活曲线亦无明显影响。对照组和模拟失重组大鼠脑基底动脉VSMCs的CaL电流密度在给予Ang Ⅱ处理后均显著增加,且模拟失重组的增加幅度显著大于对照组。以上结果提示,3d短期模拟失重即可引起大鼠脑动脉VSMCs的CaL发生适应性改变,且可导致其对Ang Ⅱ的反应性增强,表明Ang Ⅱ可能在脑动脉失重适应性改变中起着一定的作用。 Studies have shown that simulated weightlessness can cause regional changes in rat cerebral arteries, in which Ca2 + channels and renin-angio-tensin system (RAS) may play an important role. This study aimed to investigate the effects of angiotensin Ⅱ (Ang Ⅱ) on L-type calcium channel (CaL) in basal artery vascular smooth muscle cells (VSMCs) in rats under simulated short- Effect of function. After simulated weightlessness (tail suspension) for 3 days, rat basilar artery VSMCs were isolated by papain. Using whole cell patch clamp technique, the current density of CaL was determined by using Ba2 + as a carrier, and then the effect of Ang Ⅱ on this current was observed. The results showed that simulated weightlessness 3d had no significant effect on the membrane capacitance and access resistance of basilar artery VSMCs in rats, but the CaL current density of VSMCs significantly increased. However, simulated weightlessness also had no significant effect on the voltage-activated and steady-state activation curves of CaL. The CaL current density of basilar artery VSMCs in control and simulated weightless rats increased significantly after Ang Ⅱ treatment, and the increase in simulated weightlessness rats was significantly greater than that in control rats. The above results suggest that 3d short-term simulated weightlessness can induce the adaptive changes of CaL in rat cerebral arteries and lead to its increased responsiveness to Ang Ⅱ, indicating that Ang Ⅱ may play a role in the adaptive changes of cerebral arterial weightlessness Role.