Cl-通道阻断剂对A10细胞α1-AR介导的Ca2+内流的影响

目的 :在胚胎大鼠主动脉平滑肌细胞 (A10 ) ,探讨Cl- 通道与Ca2 + 内流的关系及酪氨酸磷酸化对Ca2 + 内流的作用。方法 :采用Fura 2荧光探针双波长测定胞浆游离Ca2 + 浓度 (Ca2 + ]i)。结果 :Ca2 +通道阻断剂nifedipine和SK&F96 36 5可阻止肾上腺素 (Adr)触发的Ca2 + 内流 ;氯通道阻断剂niflumicacid(NFA)和furosemide呈浓度依赖性抑制Ca2 + 内流。在Ca2 + 内流被SK&F96 36 5最大限度抑制后 ,NFA和furosemide可进一步抑制Ca2 + 内流 ;而Ca2 +内流被NFA和furosemide分别最大抑制 2 8%和 35 %后 ,SK&F96 36 5也可进一步抑制Ca2 + 内流达 5 3%和5 2 %。genistein呈浓度依赖性抑制Ca2 + 内流 ;vana date浓度依赖性促进Ca2 + 内流。结论 :在A10细胞 ,肾上腺素受体触发的Ca2 + 内流涉及电压依赖性Ca2 + 通道 (VDC)和受体操纵性Ca2 + 通道 (ROC) ;氯通道参与了VDC及ROC介导的Ca2 + 内流 ;蛋白酪氨酸磷酸化的水平影响Ca2 + 内流。

Effects of chloride channels blockers on Ca2 + influx induced by adrenoline in A1O cells1

AIM: To investigate the relationship between chloride channels and the Ca 2+influx induced by adrendine(Adr). METHODS: The effects of drugs on Adr-induced Ca 2+influx were investigated with Fura-2 fluorescence technique. RESULTS: Adr-induced Ca 2+influx was inhibited by nifedipine,SK&F96365,NFA and furosemide in a concentration manner respectively; Ca 2+influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 also could further inhibit the Ca 2+influx which had been inhibited by NFA or furosemide. Genistein and vanadate could reduce or increase the Ca 2+influx respectively. CONCLUSION: Ca 2+influx induced by Adr is related to VDC and ROC, and chloride channels involves in the processes.The levels of tyrosine phosphoralation affect the Ca 2+influx.