【摘要】 目的探讨尾加压素Ⅱ(UrotensinⅡ,UⅡ)对肾小球系膜细胞(GMC)内游离钙浓度的影响及其作用机制。方法以体外培养的SD乳鼠GMC为研究对象,用UⅡ刺激GMC,Fluo3/AM荧光标记细胞内游离钙离子,激光共聚焦显微技术动态测定GMC内游离钙浓度变化。结果UⅡ激发GMC内[Ca2+]i升高作用分2个时相,即瞬时峰值升高时相和缓慢持久升高时相,对峰值升高呈剂量依赖方式,在10-10mol/L~10-7mol/L范围内引起峰值升高,且随着剂量增加,幅度增大。硝苯地平和无钙缓冲液对UⅡ激发GMC内[Ca2+]i瞬时峰值升高无作用,但可完全阻止缓慢持久升高时相出现。结论UⅡ激发GMC内[Ca2+]i浓度瞬时峰值升高时相是由细胞内储存钙释放介导的,而缓慢持久升高时相是由细胞外钙流入增加引起的。更多还原

【Abstract】 Objective To explore the effect of urotensin Ⅱ（UⅡ） on cytosolic free calcium([Ca²⁺]i) in glomerular mesangial cells（GMC） and to investigate its involving mechanism.Methods Mesangial cells of neonatal Sprague-Dawley rats were cultured and stimulated with UⅡ.The change of [Ca²⁺]i in mesangial cells were marked with Fluo3/AM fluorescent probe and detected by a confocal microscope through laser scanning.Results The effect of urotensin Ⅱ on cytosolic free calcium [Ca²⁺]i was expressed in two phases.The first was a transient peak increase of [Ca²⁺]i and the second was a sustained increase of [Ca²⁺]i in mesangial cells.The transient peak [Ca²⁺]i phase was dose-dependent on the UⅡ concentration which changed from 10^-10mol/L to 10^-7mol/L,and the greater dosage,the higher the transient peak increase in [Ca²⁺]i.Nifedipine and buffer solution without Ca²⁺ had no effect on the transient peak phase but stopped completely the sustained increase of [Ca²⁺]i which evoked by urotensin Ⅱ.Conclusions These findings indicate that the transient peak increase of [Ca²⁺]i phase evoked by UⅡ is mediated by release of intracellular store of [Ca²⁺]i and the sustained increase of [Ca²⁺]i is caused by influx of extracellular Ca²⁺.更多还原