Yazawa H, Iida-Kubota E, Honda K
Drug Serendipity Research Laboratories, Yamanouchi Pharmaceutical Co., Ltd., Tokyo, Japan.
Jpn J Pharmacol. 1993 Aug;62(4):339-43. doi: 10.1254/jjp.62.339.
We characterized the angiotensin II (AII) receptor in human aortic smooth muscle cells (HASMCs). This receptor binds [125I]Sar1,Ile8-angiotensin II with a high affinity of 0.20 +/- 0.04 nM and a low capacity of 5.3 +/- 0.4 fmol/mg protein (230 +/- 17 sites/cell). Based on the Ki values, the ranking order of [125I]Sar1,Ile8-AII binding inhibition was as follows: Sar1,Ile8-AII > AII > Dup 753 > AII > AI >> PD 123319. The addition of AII to HASMCs induced a rapid, transient increase in intracellular free Ca2+ concentration followed by a lower, sustained phase. When extracellular Ca2+ was removed by adding 3 mM EGTA, this initial transient increase was not changed, but the sustained phase was abolished. These results revealed AII receptors in HASMCs to be of the type 1 receptor subtype, which induce Ca2+ mobilization mainly from intracellular Ca2+ stores.
我们对人主动脉平滑肌细胞（HASMCs）中的血管紧张素II（AII）受体进行了表征。该受体以0.20±0.04 nM的高亲和力和5.3±0.4 fmol/mg蛋白质的低容量（230±17个位点/细胞）结合[125I]Sar1，Ile8 - 血管紧张素II。根据Ki值，[125I]Sar1，Ile8 - AII结合抑制的排序如下：Sar1，Ile8 - AII > AII > Dup 753 > AII > AI >> PD 123319。向HASMCs中添加AII会导致细胞内游离Ca2+浓度迅速、短暂升高，随后是较低的持续阶段。当通过添加3 mM EGTA去除细胞外Ca2+时，这种最初的短暂升高没有变化，但持续阶段被消除。这些结果表明，HASMCs中的AII受体属于1型受体亚型，其主要从细胞内Ca2+储存中诱导Ca2+动员。
