摘要
ET-1激发肾小球系膜细胞(glomerularmesangialcell,GMC)内[Ca2+]i;升高作用分2个时相,即瞬时峰值升高和缓慢持久升高,对峰值升高呈剂量依赖方式,<10-10mol/L不引起峰值升高,≥10-10mol/L引起峰值升高,且随着剂量增加,幅度增大。维拉帕米对ET-1激发GMC内[Ca2+]i峰值升高和持久升高均无抑制作用;细胞内储存钙释放抑制剂TMB-8明显抑制峰值升高,但对持久升高无作用;无钙缓含冲液(1mol/LEGTA处理)对峰值升高无作用,但可完全阻止持久升高作用。结果表明ET-1激发GMC内[Ca2+]i浓度峰值升高是由细胞内储存钙释放介导的,而持久升高是由细胞外钙流入增加引起的。
The effect of endothelin - 1 on cytosolic free calcium ([Ca2+ ],) was expressed in two phases, the first was a transient peak increase in [Ca2+ ] i and the second a sustained increase in [Ca2+]i. The transient peak [Ca2+]i was dose- dependent, doses of ET- 1<10-10mol/L did not evoke transient peak increase, while≥10-10mol/L evoked transient peak increase and the greater the ET - 1 dosage, the higher the transient peak increase in [Ca2+]i. Verapamil (10-5mol/L) had no effect on the transient peak and the sustained increase in [Ca2+]i evoked by ET- 1, TMB - 8, an inhibitor of intracellular stored Ca2+ release, inhibited significantly the transient peak increase, but had no effect on the sustained increase in [Ca2+]i evoked by ET - 1; a buffer solution devoid of Ca2+ had no effect on the transient peak but abolished completely the sustained increase in [ Ca2+]i evoked by ET- 1. These findings indicated that the transient peak increase in [Ca2+]i evoked by Et- 1 was mediated by release of intracellular store of Ca2+ and the sustained increase in [Ca2+]i was caused by extracellular Ca2+ influx.
出处
《上海第二医科大学学报》
CSCD
1997年第3期185-187,共3页
Acta Universitatis Medicinalis Secondae Shanghai
关键词
内皮素-1
肾小球系膜细胞
钙
endothelin-1
glomerular mesangial cell
cytosolic free calcium