摘要
目的：分析高钾离子（Ｋ＋）引起ＰＣ１２细胞内游离钙离子浓度（［Ｃａ２＋］ｉ）升高的可能机制。方法：利用ＭｉｒａＣａｌＩｍａｇｅＳｙｓｔｅｍ检测［Ｃａ２＋］ｉ，Ｃａ２＋荧光探针为Ｆｕｒａ－２／ＡＭ。结果：（１）ＫＣｌ浓度为３０～１００ｍｍｏｌ／Ｌ时，可剂量依赖性地诱导ＰＣ１２细胞［Ｃａ２＋］ｉ升高；（２）在细胞外无Ｃａ２＋时，高Ｋ＋对ＰＣ１２细胞［Ｃａ２＋］ｉ无影响；（３）Ｌ－型电压门控钙通道阻滞剂维拉帕米、地尔硫和硝苯地平的浓度分别为５×１０－５，１×１０－４和５×１０－３ｍｏｌ／Ｌ时，可完全阻断高Ｋ＋诱导的ＰＣ１２细胞［Ｃａ２＋］ｉ升高，但Ｎ－型电压门控钙通道阻滞剂ω－ｃｏｎｏｔｏｘｉｎＧＶＩＡ在浓度为１×１０－６ｍｏｌ／Ｌ时，对高Ｋ＋诱导的ＰＣ１２细胞［Ｃａ２＋］ｉ升高没有影响；（４）５×１０－５ｍｏｌ／Ｌ维拉帕米对细胞外由无Ｃａ２＋到有Ｃａ２＋过程引起的［Ｃａ２＋］ｉ升高无抑制作用。结论：高Ｋ＋引起ＰＣ１２细胞［Ｃａ２＋］ｉ升高以细胞质膜上Ｌ－型电压门控Ｃａ２＋通道开放为基础。
Objective: To elucidate the mechanism of [Ca^(2+)]i rise induced by highK^+ concentration in PC12 cells. Methods: [Ca^(2+)]i was assayed with MiraCal Image System using Fura2/AM as Ca^(2+)fluorescence probe. Results: (1) In PC12 cells KCl at 30～100 mmol/L could induce [Ca^(2+)]i rise in concentration dependent manner. (2) In PC12 cells KCl at 55 mmol/L could not induce [Ca^(2+)]i change in extracellular Ca^(2+)free condition. (3) It was found that verapamil, diltiazem and nifedipine at 5×10-5, 1×10-4and 5×10-3 mol/L, respectively, could inhibit completely [Ca2+]i rise induced by highK^+. But ωconotoxin GVIA at 1×10-6mol/L showed no influence on [Ca^(2+)]i rise induced by highK+. (4) Verapamil at 5×10-5 mol/L was ineffective on [Ca^(2+)]i rise induced by addition of CaCl2 to extracellularCa^(2+)free condition. Conclusion: The increase of [Ca^(2+)]i in response to KCl stimulation in PC12 cells was determined by the open of L-type voltagegated calcium channels, N-type voltagegated calcium channels and the leak influx of Ca^(2+) were not involved in [Ca^(2+)]i rise induced by highK^+ in PC12 cells.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1998年第4期343-346,共4页
Academic Journal of Second Military Medical University
基金
国家自然科学基金
关键词
PC12细胞
高钾离子
钙离子
浓度
PC12 cells
high concentration K^+
intracellular free Ca^(2+) concentration
