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目的观察模拟失重2周后,大鼠脑动脉血管平滑肌细胞(vascular smooth muscle cells,VSMCs)L型电压依赖性钙离子通道(L-type voltage dependent calcium channel,CaL)功能的改变,以及钙通道激动剂BayK8644对通道电流的影响。方法以尾部悬吊大鼠模型模拟失重的影响。采用全细胞膜片钳记录模式,以Ba2+作为载流子,记录2周模拟失重后大鼠脑动脉VSMCs的CaL电流及钙通道激动剂Bay K 8644对其的影响,并测定相应的稳态激活与失活曲线及有关参数。结果与对照组相比,模拟失重2周后悬吊组大鼠已出现了典型的模拟失重效应,悬吊组大鼠脑动脉VSMCs的CaL的电流密度显著增加(P<0.05),且对钙通道激动剂Bay K 8644更敏感(P<0.05)。此外,与对照组相比,悬吊组大鼠脑动脉VSMCs的膜电容与接入电阻、CaL稳态失活曲线和稳态激活曲线等通道动力学特征无显著性改变。结论模拟失重2周可引起大鼠脑动脉平滑肌细胞CaL通道功能增强,这可能是模拟失重导致大鼠脑动脉血管收缩反应性增强的因素之一。
Objective To observe the changes of L-type voltage dependent calcium channel (CaL) function in rat cerebral arterial vascular smooth muscle cells (VSMCs) after 2 weeks of simulated weightlessness and the effects of calcium channel activation Effect of BayK8644 on Channel Current. Methods The tail suspension model was used to simulate the effects of weightlessness. Using whole-cell patch-clamp recording mode and Ba2 + as carrier, the CaL current of rat cerebral artery VSMCs after 2 weeks of simulated weightlessness and the effect of calcium channel agonist Bay K 8644 on them were recorded. The corresponding homeostasis activation and Inactivation curve and related parameters. Results Compared with the control group, the typical weightlessness effect appeared in the suspension group after 2 weeks of simulated weightlessness. The current density of CaL in VSMCs of the suspension group increased significantly (P <0.05) The channel agonist Bay K 8644 is more sensitive (P <0.05). In addition, compared with the control group, there was no significant change in the channel kinetic characteristics such as membrane capacitance and access resistance, CaL steady-state inactivation curve and steady-state activation curve of VSMCs in the suspension group. Conclusion Simulated weightlessness for 2 weeks can induce the enhancement of CaL channel in rat cerebral artery smooth muscle cells, which may be one of the factors that lead to the increase of cerebral vasoconstriction reactivity in rats after simulated weightlessness.