Cl-通道阻断剂对A10细胞α1-AR 介导的Ca2+内流的影响1

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&F96365 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&F96365 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 28%和 35%后, SK&F96365 也可进一步抑制 Ca²⁺ 内流达 53%和52%。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 adrenaline in A10 cells1

AIM: To investigate the relationship be-tween chloride channels and the Ca²⁺ influx induced by a-drendine(Adr).METHODS: The effects of drugs on Adr-induced Ca²⁺ influx were investigated with Fura-2 fluorescence technique.RESULTS: Adr-induced Ca²⁺ influx was inhibited by nifedipine, SK&F96365, NFA and furosemide in a concentration manner respectively; Ca²⁺ influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 also could further inhibit the Ca²⁺ influx which had been inhibited by NFA or furosemide.Genistein and vanadate could reduce or increase the Ca²⁺ influx respectively. .CONCLUSION: Ca²⁺ influx induced by Adr is related to VDC and ROC, and chloride channels involves in the processes.The levels of tyrosine phosphoralation affect the Ca²⁺ influx.