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选用α１Ｂ-肾上腺素受体（α１Ｂ－ＡＲ）密度分别为（６３３６±９１３）和（７７３±１６４）ｆｍｏｌ·ｍｇ－１的两株克隆ＨＥＫ２９３细胞，分别用高表达和低表达α１Ｂ-ＡＲ表示，比较去甲肾上腺素（ＮＥ）持续作用下不同初始表达水平的α１Ｂ－ＡＲ发生密度改变的差别．结果显示： １０μｍｏｌ·Ｌ－１ＮＥ持续作用４８ｈ可使高表达以α１Ｂ－ＡＲ的密度发生下调，却可使低表达α１Ｂ－ＡＲ的密度发生上调．蛋白激酶Ｃ（ＰＫＣ）抑制剂ＲＯ－３１－８２２０或Ｃａｌｐｈｏｓｔｉｎ Ｃ可消除ＮＥ对高表达α１Ｂ－ＡＲ的下调作用，但对低表达α１Ｂ－ＡＲ的密度上调无影响．ＰＫＣ激动剂ＰＭＡ不仅可模拟ＮＥ对高表达α１Ｂ－ＡＲ的下调作用，而且使低表达α１Ｂ－ＡＲ的密度也发生下调．肌浆网／内质网钙泵抑制剂ＣＰＡ和内钙螯合剂ＢＡＰＴＡ－ＡＭ不影响ＮＥ对高表达α１Ｂ－ＡＲ的下调作用，但可部分抑制低表达α１Ｂ－ＡＲ的上调．以上结果提示，ＮＥ持续作用可对初始表达水平不同的α１Ｂ－ＡＲ密度产生不同方向的调节作用，作用机制亦不尽相同．
Two clones of HEK293 cells with (6336 ± 913) and (773 ± 164) fmol · mg-1 α1B-adrenergic receptors (α1B-AR) were selected and identified by high and low expression of α1B- The differences in the density changes of α1B-AR at different initial expression levels were compared with the sustained effects of norepinephrine (NE). The results showed that the persistence of 10μmol·L-1NE for 48h reduced the expression of α1B-AR, while up-regulated the expression of α1B-AR. Protein kinase C (PKC) inhibitor RO-31-8220 or Calphostin C abolished the down-regulation of NE1-overexpressing α1B-AR, but had no effect on the up-regulation of low-expression α1B-AR. PKC agonist PMA can not only mimic the NE down-regulation of high expression of α1B-AR, but also down-regulate the expression of low-expression α1B-AR. The sarcoplasmic / endoplasmic reticulum calcium pump inhibitor CPA and the intracellular calcium chelator BAPTA-AM did not affect NE down-regulation of high expression of α1B-AR, but partially inhibited the up-regulation of low expression of α1B-AR. The above results suggest that sustained effects of NE may exert different regulatory effects on the density of α1B-AR with different initial expression levels, and the mechanism of action is also different.