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。
Objective To explore the effect of urotensin Ⅱ （U Ⅱ ） on cytosolic free calcium （[ Ca^2＋ ]i） in glomerular mesangial cells （GMC） and to investigate its involving mechanism. Methods Mcsangial cells of neonatal Spraguc - Dawlcy rats were cultured and stimulated with UⅡ . The change of [ Ca^2＋ ]i in mesangial ceils were marked with Fluo3/AM fluorescent probe and detected by a confocal nficroseope through laser scanning. Results The effect of urotensin H on cytosolic free calcium [Ca^2＋ ]i was expressed in two phases. The first was a transient peak increase of [ Ca^2＋ ]i and the second was a sustained increase of [ Ca^2＋ ]i in mesangial cells. The transient peak [ Ca^2＋ ]i phase was dose- dependent on the U H concentration which changed from 10^-10mol/L to 10^-7 tool/L, and the greater dosage, the higher the transient peak increase in [Ca^2＋ ]i. Nifedipine and buffer solution without Ca^2＋ had no effect on the transient peak phase but stopped completely the sustained increase of [ Ca^2＋ ] i which evoked by urotensin Ⅱ . Conclusions These findings indicate that the transient peak increase of [ Ca^2＋ ] i phase evoked by U Ⅱ is mediated by release of intracellular store of [ Ca^2＋ ] i and the sustained increase of [ Ca^2＋ ] i is caused by influx of extracellular Ca^2＋ .
出处
《现代临床医学生物工程学杂志》
2006年第2期103-105,116,共4页
Journal of Modern Clinical Medical Bioengineering
基金
广州市医药卫生科技项目(2005-YB-131)
