中文摘要：

目的：观察pH对大鼠肺动脉平滑肌细胞（PASMCs）钾电流的调控作用并探讨其机制。方法：用全细胞膜片钳技术记录在正常细胞外液和不同pH的灌流液中，PASMCs膜上电压门控性钾电流大小（Ikv），并分析了其电生理学特性的改变。结果：①胞外pH降低可快速可逆性抑制Ikv。，与对照相比（pH7.4），pH值为7.0、6.5、6.0时，＋60mV处的峰电流的抑制率分别为：16.93％±2.47％、33.03％±2.13％、41.59％±6.53％，电流一电压关系曲线右下移。②胞外pH为7.0、6.5、6.0时，使电压依赖性Gk-Em向去极化方向移动。同时使半激活电压增加。结论：在缺氧所致缺氧性肺血管收缩反应（HPV）的发生中，胞外pH的降低可参与对Ikv的调节，从而使细胞膜去极化，Ikv减小电压门控钙通道打开，平滑肌细胞收缩，这可能是缺氧导致HPV的机制之一。

英文摘要：

To study the modulation of extracellular pH on the voltage-gated potassium currents （Ikv） in isolated pulmonary artery smooth muscle cells（PASMCs）. Methods： IKv was recorded using whole-cell patch clamp technique under the external solutions with different pH. The electrophysiological characteristics of Ikv were then analyzed. Results： ①As compared to the normoxic group, IKv decreased under acidic condition. When the extracellular pH were 7.0, 6.5, 6.0, the peak currents at a potential of ＋ 60 mV were inhibited by 16.93% ±2.47%（P〈0.01）,33.03%±2.13% （P〈0.01）,41.59% ±6.53%（P〈0.01） respectively, and the cur-rent-voltage relationship（I/V） curve shifted to the right. ②When the extracellular pH was 7.0,6.5,6.0, the voltage-depended Gk-Em was shifted to the direction of positive and the activation was sped up. Conclusion： The results suggest that with the development of hypoxic pulmonary vasoconstriction（HPV）, extracellular pH may take part in the modulation of Kv channels partly, then make the cell depolarized and decrease the Kv currents, this will lead to open the L-type calcium channel and contract the pulmonary artery smooth muscle. It may be one of the mechanisms that hylaoxic leads to HPV and finallv accelerate the development of HPV.