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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。
Objective To investigate the effect of urotensin Ⅱ (UⅡ) on intracellular free calcium concentration in glomerular mesangial cells (GMC) and its mechanism. Methods GMCs from neonatal SD rats were cultured in vitro. Fluorescein-labeled intracellular free calcium (Ca (superscript 2 +)) was detected by Fluorescent staining with Fluorescence stimulated by UII and the concentration of intracellular free calcium in GMC was measured by laser confocal microscopy. Results UII stimulated the [Ca2 +] i up-regulation in GMCs in two phases: transient phase and slow phase, in a dose-dependent manner. In 10-10mol / L ~ 10 -7mol / L range caused by the peak rise, and as the dose increases, the magnitude increases. Nifedipine and calcium-free buffer had no effect on the instantaneous peak rise of [Ca2 +] i in UMC-stimulated GMC, but completely prevented the appearance of slowly and permanently elevated phase. CONCLUSION U2-stimulated [Ca2 +] i concentration in GMC is mediated by intracellular Ca2 + release during transient peak elevation, whereas Ca2 + influx is caused by increased extracellular calcium influx.