论文部分内容阅读
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。
ET-1 stimulated [Ca2 +] i in glomerular mesangial cells (GMCs). The up-time was divided into two phases, ie, transient peak and slow sustained increase, and the peak was increased in a dose- <10-10mol / L did not cause peak rise, ≥ 10-10mol / L caused peak rise, and with the dose increased, the amplitude increased. Verapamil had no inhibitory effect on the peak and prolonged elevation of [Ca2 +] i in GMC stimulated by ET-1; TMB-8, an inhibitor of intracellular calcium release, significantly inhibited peak elevation but had no effect on persistent increase ; Calcium-free buffer solution (1mol / LEGTA treatment) had no effect on peak rise, but could completely prevent the long-lasting increase. The results show that the peak of [Ca2 +] i concentration in GMC stimulated by ET-1 is mediated by the release of intracellular calcium, while the persistent increase is caused by extracellular calcium influx.