研究人Ｂ细胞电压依赖性钾通道（Ｋｖ） 及ＡＴＰ敏感性Ｃｌ－ 通道的存在及其调节。以人Ｂ细胞（Ｄａｕｄｉｃｅｌｌｓ）为研究对象，膜片钳技术做全细胞记录。结果表明，①全细胞ｖｏｌｔａｇｅｒａｍｐｐｒｏｔｏｃｏｌ 证实有Ｋｖ 通道的存在，该Ｋｖ 通道对钾通道阻断剂ｑｕｉｎｉｎｅ １００μｍｏｌ·Ｌ－ １ 及ｃｈａｒｙｂｄｏｔｏｘｉｎ（ＣＴＸ）１００ｎｍｏｌ·Ｌ－ １ 敏感。②灌流液中加入ＡＴＰ１ｍｍｏｌ·Ｌ－ １ 后，Ｋｖ 失活，并激活一外向性整流电流。在有ｑｕｉｎｉｎｅ 或ＣＴＸ存在时，该外向性电流仍然存在，但可被Ｃｌ－ 通道阻断剂ＤＩＤＳ１００μｍｏｌ·Ｌ－ １ 及Ｐ２ 受体阻断剂ｓｕｒａｍｉｎ １００μｍｏｌ·Ｌ－ １ 阻断。③电极液中加入ＰＩＰ２ ５μｍｏｌ·Ｌ－ １ ，也可明显削弱该外向性电流。提示人Ｂ细胞膜上有Ｋｖ 通道及ＡＴＰ敏感性Ｃｌ－ 通道的表达，Ｐ２ 受体及ＰＩＰ２ 可能参与其信息转导过程。 To study the existence and regulation of human B cell voltage-dependent potassium channels (Kv) and ATP-sensitive Cl-channels. Human B cells (Daudicells) as the research object, patch-clamp technique to do whole-cell recording. The results showed that: ① whole cell voltage  rampprotocol confirmed the existence of Kv channels, the Kv channel potassium channel blockers quinine 100μmol·L-1 and charybdotoxin (CTX) 100nmol·L-1 sensitive. ② After adding ATP1mmol·L-1 into the perfusate, Kv was inactivated and an outward rectifier current was activated. The outward current was still present in the presence of quinine or CTX but was blocked by Cl-channel blocker DIDS 100 μmol·L -1 and the P2 receptor blocker suramin 100 μmol·L -1. ③ PIP2 electrode solution added 5μmol·L-1, but also significantly weakened the outward current. Suggesting that human B cell membrane Kv channel and ATP-sensitive Cl-channel expression, P2 receptor and PIP2 may be involved in its information transduction process.