模拟失重1周大鼠脑动脉平滑肌细胞BK_(Ca)与K_V通道功能的改变

Functional alterations in BK_(Ca) and K_V channels of cerebrovascular myocytes from rat underwent 1-wk simulated microgravity

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 investigate the functional changes of large conductance Ca^2＋ -activated potassium channel （BKCa） and voltage-gated potassium channel （Kv） in vascular smooth muscle cells （VSMCs） isolated from cerebral arteries of rats after a short-term simulated microgravity. Methods Male Sprague-Dawley rats were subjected to 1-wk tail suspension （SUS） to simulate cardiovascular deconditioning due to microgravity. With intracellular Ca^2＋ being kept within physiological range, the BKCa and Kv currents and resting membrane potential were recorded and determined using conventional whole-cell voltage-clamp technique. Results The myocytes from SUS rats had a more depolarized membrane potential and a greater BKCa current density as compared with those from control rats. However, the Kv current density of SUS myocytes showed diverse changes related to the testing potential： it was greater at -20 ～＋20 mV and became smaller at ＋50～ ＋60 mV as compared with the controls. Conclusions These findings suggest that the alterations in function of BKCa and Kv channels of cerebral VSMCs might be involved in the electrophysiological mechanisms that mediate the increased vasoreactivity and hypertrophic change in cerebral arteries during adaptation to microgravity.