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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。
OBJECTIVE: To investigate the relationship between Cl-channel and Ca2 + influx and the effect of tyrosine phosphorylation on Ca2 + influx in aortic smooth muscle cells of embryonic rat (A10). Methods: Cytosolic free Ca2 + concentration ([Ca2 +] i) was measured by Fura 2 fluorescent probe dual wavelength. RESULTS: Ca 2+ channel blockers nifedipine and SK & F96 36 5 blocked adrenergic (Ca 2+) -induced Ca 2+ influx. Chloride channel blockers niflumicacid (NFA) and furosemide inhibited Ca 2+ influx in a concentration-dependent manner. After Ca2 + influx was maximally inhibited by SK & F96 365, NFA and furosemide further inhibited Ca2 + influx; however, SK & F96 36 5 was also inhibited after Ca2 + influx was maximally inhibited by 28% and 35%, respectively, by NFA and furosemide Further inhibition of Ca 2+ influx reached 53% and 52%. Genistein inhibited Ca2 + influx in a concentration-dependent manner; vana date promoted Ca2 + influx in a concentration-dependent manner. CONCLUSION: Adrenoceptor-triggered Ca2 + influx in A10 cells involves voltage-dependent Ca2 + channels (VDCs) and receptor-manipulated Ca2 + channels (ROCs). Chloride channels are involved in VDC and ROC-mediated Ca2 + Influx; Protein tyrosine phosphorylation affects Ca2 + influx.