目的:探讨顺铂激活的低分化鼻咽癌细胞(CNE-2Z)氯通道电流是否为钙激活的氯电流。方法:采用膜片钳全细胞记录技术记录细胞内/外无Ca2+及钙通道阻断剂对顺铂激活氯电流的影响,并用高渗灌流液观察顺铂激活氯电流的容积敏感性。结果:去除细胞外液的Ca2+后,5μmol/L顺铂能诱发氯电流,且电流大小与细胞外有Ca2+时无明显差异,但潜伏期与达峰时间延长。细胞内外均无Ca2+对顺铂激活氯电流未产生影响。钙通道阻断剂nifedipine未能抑制顺铂诱发的氯电流。但细胞外灌流高渗液几乎可完全抑制顺铂激活的氯电流。结论:顺铂激活的氯通道开放不依赖于细胞内/外的Ca2+,该通道不是钙激活氯通道而很可能是容积敏感性氯通道。 Aims: To investigate whether the chloride channel current of cisplatin-activated poorly differentiated nasopharyngeal carcinoma cells (CNE-2Z) is a calcium-activated chloride current. Methods: Whole-cell patch-clamp recording technique was used to record the effects of intracellular Ca 2+ and Ca 2+ channel blockers on cisplatin-activated chloride currents. The volume sensitivity of cisplatin-activated chloride currents was observed by high perfusion perfusate. Results: After removing Ca2 + from extracellular fluid, 5μmol / L cisplatin could induce the chloride current, and there was no significant difference between the current and the extracellular Ca2 + concentration. However, the incubation period and peak time were prolonged. No intracellular Ca2 + on cisplatin-activated chloride current did not affect. The calcium channel blocker nifedipine failed to inhibit cisplatin-induced chloride currents. However, extracellular perfusion of hypertonic fluid almost completely inhibited cisplatin-activated chloride current. CONCLUSIONS: Cisplatin-activated chloride channel opening is independent of intracellular / extracellular Ca2 +, which is not a calcium-activated chloride channel and is probably a volume-sensitive chloride channel.