目的探讨氯通道阻断剂在α１Ａ、α１Ｂ、α１Ｄ肾上腺素受体（ＡＲ）亚型触发的Ｃａ２＋内流中的作用。方法采用Ｆｕｒａ－２荧光探针双波长测定胞浆游离Ｃａ２＋浓度（［Ｃａ２＋］ｉ）。结果在３种亚型的细胞上，肾上腺素（Ａｄｒ）触发的Ｃａ２＋内流均不受ｎｉｆｅｄｉｐｉｎｅ影响； ＳＫ＆Ｆ９６３６５可部分抑制α１Ａ、α１Ｂ－ＡＲ介导的Ｃａ２＋内流，而对ａ１Ｄ－ＣＨＯ细胞无影响。在ＢＢ－ＣＨＯ细胞上，ｎｉｆｌｕｍｉｃａｃｉｄ（ＮＦＡ）和ｆｕｒｏｓｅｍｉｄｅ呈浓度依赖性抑制Ｃａ２＋内流；当Ｃａ２＋内流被ＳＫ＆Ｆ９６３６５最大限度抑制后，ＮＦＡ和ｆｕｒｏｓｅｍｉｄｅ可进一步抑制Ｃｄ２＋内流。α１Ａ－ＡＲ介导的Ｃａ２＋内流可被ｆｕｒｏｓｅｍｉｄｅ抑制，抑制率达 １４％ １５％。 ＮＦＡ可抑制ａ１Ｄ－ＡＲ引起的Ｃａ２＋内流，抑制率为３９％±９％。结论氯通道参与α１Ａ、α１Ｂ及α１Ｄ－ＡＲ引起的经非电压依赖性Ｃａ２＋通道介导的Ｃａ２＋内流，其间存有异同。ＮＦＡ敏感Ｃａ２＋内流及ｆｕｒｏｓｅｍｉｄｅ敏感的Ｃａ２＋内流与ＳＫ＆Ｆ９６３６５敏感的Ｃａ２＋内流存在非同一性。

　　AIM To investigate the roles of Cl- channels in Ca2+ influx induced by activaion of al- adrenoceptor subtypes in transfected-CHO cells. METHODS The effects of drugs on α1A、α1B and α1D- AR-induced Ca2+ influx were investigated with Fura2 fluorescence technique. RESULTS The α1A-AR- induced Ca2+ influx was inhibited by furosemide(2 .5 ~ 10 Mμmol·L- 1 )and SK&F96365(5- 15 μmol·L- 1 ) in a concentration- dependent manner respectively; The α1B-AR-induced Ca2+ influx could also be inhibit inhibited by NFA(2. 5 ...