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本文用膜片箝全细胞技术比较研究了单个兔肺动脉血管平滑肌细胞上延迟整流钾通道与克隆Kv1．5通道的电生理及药理学特性。将平滑肌细胞箝制在-40mV，以10mV的步距阶跃去极化（0～60mV）可产生一系列快速上升的外向电流，几无衰减，其激活曲线的V1/2为27．2mV。灌流液中加入100mmol／LTEA和1mmol／L 4AP，电流幅度均明显减小，细胞外Ca2+水平由1．5mmol／L降至0．5mml／L甚至0mmol／L时，该电流无明显改变。而在HBK7细胞（克隆Kv1．5通道），箝制在－80mV，以10mV的步距阶跃去极化（－30～＋60mV），可产生一系列的快速上升的外向电流，激活更快，无衰减，其激活曲线的V1/2为0．8mV。4AP抑制Kv1．5的IC50为7．3mmol／L，呈现频率和使用非依赖性；TEA30，100，300mmol／L分别使该电流幅度下降28.6％，37.4％，46．3％，Quinidine0．1和1mmol／L使其下降29．7％，37．6％。研究表明，我们记录到急性分离的免血管平滑肌细胞延迟整流钾通道，它的电生理及药理学特性与克隆的Kv1．5延迟整流钾通道存在明显差别。
In this paper, patch clamp whole cell technology was used to compare the electrophysiological and pharmacological properties of delayed rectifier potassium channel and clone Kv1.5 channel in a single rabbit pulmonary artery smooth muscle cell. Clamping smooth muscle cells at -40mV and depolarizing (0 ~ 60mV) with 10mV step-by-step results in a series of rapidly rising outward currents with almost no decay and a V1 / 2 of 27.2mV activation curve. The current amplitude was significantly decreased when 100 mmol / L EDTA and 1 mmol / L 4AP were added into the perfusate solution. No significant changes were observed in the extracellular Ca2 + levels from 1.5 mmol / L to 0.5 mmol / L or even 0 mmol / L. In HBK7 cells (cloned Kv1.5 channels), clamp-down at -80 mV and step-depolarization (-30 to +60 mV) at 10 mV steps produces a series of rapidly rising outward currents that activate faster, Attenuation, its activation curve V1 / 2 0.8mV. 4AP inhibited the IC50 of Kv1.5 to 7.3mmol / L, showing the frequency and the use of independence; TEA30,100,300mmol / L decreased the current amplitude of 28.6%, 37.4%, 46.3%, Quinidine0.1 and 1mmol / L decreased 29.7%, 37.6%. Studies have shown that we documented an acutely isolated delayed rectifier potassium channel in rat vascular smooth muscle cells whose electrophysiological and pharmacological properties differed significantly from the cloned Kv1.5 delayed rectifier potassium channel.