Cl~-通道及Ca~(2+)通道阻断剂对ATP触发的牛脑血管平滑肌细胞Ca~(2+)内流作用的影响

采用Fura 2荧光测定胞浆游离Ca2 + 浓度(Ca2 + ]i)变化技术 ,在培养的牛脑中动脉平滑肌细胞上 ,观察电压依赖Ca2 + 通道 (VDCC)抑制药尼莫地平 ,非电压依赖Ca2 + 通道 (NVDCC)SK&F96365以及Cl-通道抑制药呋塞米 ,印防己毒素对ATP引起的Ca2 + ]i 反应的影响 .实验表明ATP可使 Ca2 + ]i 呈现双相升高反应 ,即快速峰相及随后持续稳定的平台相 .尼莫地平 ,SK&F96365及印防己毒素对ATP触发的Ca2 + 内流无明显影响 ,而呋塞米能呈浓度依赖性地抑制ATP触发的Ca2 + 内流 .提示ATP触发的牛脑中动脉平滑肌细胞Ca2 + 内流是经SK&F96365不敏感的NVDCC ,与呋塞米敏感的Cl- 通道开放有关 .

Effects of Cl- and Ca2+ channels blockers on ATP-induced Ca2+ influx in cultured calf middle cerebral artery smooth muscle cells

In order to understand the ATP-induced Ca²⁺ influx characterization, we studied the effects of Ca²⁺ channel blockers(nimodipine and SK&;F96365) and Cl^- channel blockers(furosemide and picrotoxin) on ATP- induced influx in cultured calf middle cerbral artery smooth muscle cells, with Fura-2 fluorescence technique. ATP evoked the increase in cytoplasmic Ca²⁺(［Ca²⁺］_i) level. The response to ATP was biphasic, a transient peak followed by a sustained plateau. This sustained plateau was not significantly reduced by (1) voltage-dependent Ca²⁺ channel(VDCC) blocker nimodipine; (2) receptor-operated Ca²⁺ channel(ROCC) blocker SK&;F96365; (3) Cl^- channel blocker picrotoxin. However, it was significantly inhibited by furosemide in a concentration-dependent manner. These data suggest that ATP-induced Ca²⁺ influx be related to NVDCC, which is not sensitive to SK&;F96365, instead of the VDCC, and furosemide-sensitive Cl^- channel is related to this Ca²⁺ influx.