Kalenga M K, de Gasparo M, Thomas K, De Hertogh R
Department of Obstetrics and Gynecology, University of Louvain, Brussels, Belgium.
Eur J Pharmacol. 1994 Jul 15;268(2):231-6. doi: 10.1016/0922-4106(94)90193-7.
The purpose of this work was to determine which subtype of angiotensin II receptors was involved in angiotensin II-induced human placental lactogen (hPL) and pregnancy-specific beta 1-glycoprotein (SP1) secretion from human placenta. The experiments were performed using placental explants and isolated trophoblast cells. They were pretreated with Dup753 (antagonist of angiotensin AT1 receptor), PD123319 (antagonist of AT2 subtype) or with CGP42112A (agonist of angiotensin AT2 receptor) before the addition of angiotensin II. The octapeptide angiotensin II significantly increased the hPL and SP1 release from both placental explants and isolated trophoblast cells. The angiotensin AT1 receptor antagonist Dup753 inhibited the angiotensin II-stimulated hPL and SP1 secretion in a dose-dependent manner but the AT2 specific ligands PD123319 and CGP42112A had no effect. This study indicates that the angiotensin AT1 receptor is the main mediator of angiotensin II in the stimulation of hPL and SP1 secretion from human placenta.
本研究的目的是确定血管紧张素II受体的哪种亚型参与血管紧张素II诱导的人胎盘催乳素（hPL）和妊娠特异性β1-糖蛋白（SP1）从人胎盘的分泌。实验使用胎盘外植体和分离的滋养层细胞进行。在添加血管紧张素II之前，先用Dup753（血管紧张素AT1受体拮抗剂）、PD123319（AT2亚型拮抗剂）或CGP42112A（血管紧张素AT2受体激动剂）对它们进行预处理。八肽血管紧张素II显著增加了胎盘外植体和分离的滋养层细胞中hPL和SP1的释放。血管紧张素AT1受体拮抗剂Dup753以剂量依赖的方式抑制血管紧张素II刺激的hPL和SP1分泌，但AT2特异性配体PD123319和CGP42112A没有作用。这项研究表明，血管紧张素AT1受体是血管紧张素II刺激人胎盘分泌hPL和SP1的主要介质。
