目的本研究旨在探讨酰胺类局部麻醉药罗哌卡因对外源表达的大鼠脑型(rNav1.2)和心肌型(rNav1.5)电压门控钠通道电流的药理调制作用。方法运用双电极和膜片钳全细胞记录技术记录全细胞电流。结果罗哌卡因能以浓度和频率依赖的方式抑制rNav1.2和rNav1.5亚型通道的峰钠电流,其中Nav1.5亚型通道对罗哌卡因的敏感性相对较高。此外,罗哌卡因能使rNav1.2和rNav1.5亚型通道的稳态失活曲线向超极化方向显著偏移,但对激活曲线没有影响。通过重复高频去极化刺激,罗哌卡因能以使用依赖性的方式抑制rNav1.2和rNav1.5亚型通道的电流。结论结果提示罗哌卡因的药理机制体现在对钠通道亚型失活态的调制上。该结果有助于进一步理解罗哌卡因对脑型和心肌型电压门控钠通道的药理调制作用。 Objective To investigate the pharmacological modulatory effects of ropivacaine, an amide local anesthetic, on voltage-gated sodium channel currents of rat brain-type (rNav1.2) and cardiotype (rNav1.5). Methods Whole-cell currents were recorded by whole-cell recording technique with two-electrode and patch-clamp. Results Ropivacaine could inhibit the peak sodium current of rNav1.2 and rNav1.5 subtypes in a concentration-and frequency-dependent manner. The sensitivity of rAAV1.5 channel to ropivacaine was relatively high. In addition, ropivacaine caused a significant shift in the steady-state inactivation curves of the rNav1.2 and rNav1.5 subtypes towards hyperpolarization but had no effect on the activation curves. By repeating high-frequency depolarization stimulation, ropivacaine inhibits the currents in the rNavl.2 and rNavl.5 subtype channels in a usage-dependent manner. Conclusions The results suggest that the pharmacological mechanism of ropivacaine is reflected in the modulation of sodium channel subtypes inactivation. This result helps to further understand the pharmacological modulation of ropivacaine on brain-type and cardiac-type voltage-gated sodium channels.