SKF96365和氯化镍对环匹阿尼酸诱导的大鼠PASMC［Ca2＋］i升高的影响

目的：研究SKF96365和氯化镍（NiCl2）对环匹阿尼酸（CPA）诱导的大鼠远端肺动脉平滑肌细胞（PASMC）内游离钙离子浓度（Ca2＋]i）变化的影响。方法培养大鼠PASMC，运用荧光显微镜和InCyte细胞内钙浓度检测系统观测CPA、SKF96365和NiCl2对PASMCCa2＋]i的影响。结果含5μmol／L硝苯地平的无钙Krebs溶液孵育PASMC，10μmol／LCPA使PASMCCa2＋]i短暂小幅升高，恢复细胞外Ca2＋至2．5mmol／L后，10μmol／LCPA使PASMCCa2＋]i迅速显著升高；50μmol／LSKF96365和500μmol／LNiCl2均能明显抑制10μmol／LCPA引起的PASMCCa2＋]i升高，但对高钾（60mmol／LKCl）溶液引起的PASMCCa2＋]i升高无影响。结论CPA可致大鼠PASMCCa2＋]i升高，且能被SKF96365和NiCl2阻断，提示CPA可能诱发细胞外Ca2＋经钙池操纵性钙通道（SOCC）内流，SKF96365和NiCl2能选择性抑制SOCC活性使经SOCC的Ca2＋内流减少。

Effect of SKF96365 and NiCl2 on cyclopiazonic acid induced intracellular calcium cation concentration increase in rat distal pulmonary arterial smooth muscle cells

Objective To study the effect of SKF96365 and NiCl2 on cyclopiazonic acid (CPA) induced intracellular calcium cation concentration (Ca2+ ]i ) change in rat distal pulmonary arterial smooth muscle cells (PASMC) .Methods The rat distal PASMC were isolated and cultured .The effects of CPA ,SKF96365 and NiCl2 on Ca2+ ]i in PASMC were tested by fluorescence microscope and InCyte Ca2+ ]i measurement system .Results PASMC were incubated with Ca2+‐free Krebs solution containing 5μmol/L nifedipine ,10 μmol/L CPA caused a small transient increase in Ca2+ ]i ;after restoration of extracellular Ca2+ to 2 .5 mmol/L ,10 μmol/L CPA caused marked increases in Ca2+ ]i in PASMC incubated with Krebs solution containing 5 μmol/L nife‐dipine .Both 50 μmol/L SKF96365 and 500 μmol/L NiCl2 distinctly attenuated the increases in Ca2+ ]i caused by 10 μmol/L CPA in PASMC .However ,neither 50 μmol/L SKF96365 nor 500 μmol/L NiCl2 affected the increases in Ca2+ ]i caused by 60 mmol/L KCl in PASMC .Conclusion CPA induced increases in Ca2+ ]i may related to Ca2+ release from sarcoplasmic reticulum and the in‐flux of Ca2+ through store‐operated Ca2+ channels (SOCC) in rat distal PASMC .Both SKF96365 and NiCl2 could selectively block SOCC and attenuated the influx of Ca2+ through SOCC in PASMC .