论文部分内容阅读
目的探讨人α_(1D)-肾上腺素受体(α_(1D)-adrcnerslcreceptor,α_(1D)-AR)触发细胞的Ca(2+)释放和Ca(2+)内流机制。方法:将编码人α_(1D)-ARcDNA转染到缺乏α1-AR的中国仓鼠卵巢(CHO)细胞,建立稳定表达纯一α_(1D)-AR的细胞系。采用Fura-2技术观察细胞胞浆Ca(2+)浓度变化。结果:肾上腺素激活α_(1D)-AR后既触发了CHO细胞的Ca(2+)释放又引起细胞外Ca(2+)内流。磷脂酶C(phospholipaseC,PLC)抑制剂U-73122抑制α_(1D)-AR激发Ca(2+)释放的同时也抑制了Ca(2+)内流。结论:人α_(1D)-AR与PLC激活途径相耦联释放细胞内储存Ca(2+)并通过“充电式Ca(2+)内流”机制触发细胞外Ca(2+)内流。
Objective To investigate the mechanism of Ca (2+) release and Ca (2+) influx in human α 1D adrenoceptor (α 1D) -adrcnerslcreceptor and α 1D -AR. Methods: Human α 1D -AR cDNA was transfected into Chinese hamster ovary (CHO) cells deficient in α1-AR to establish a cell line stably expressing α1-AR. Fura-2 technique was used to observe the change of cytoplasmic Ca2 + concentration. Results: Activation of α1D-AR by epinephrine not only triggered the release of Ca2 + from CHO cells but also caused the influx of extracellular Ca2 +. U-73122, an inhibitor of phospholipase C (PLC), inhibits the release of Ca (2+) from α 1D-AR and inhibits Ca 2+ influx. CONCLUSION: Human α1D-AR is coupled with PLC activation pathway to release intracellular Ca2 + and triggers extracellular Ca2 + influx via “charged Ca2 + influx” mechanism.