Glance D G, Elder M G, Bloxam D L, Myatt L
Am J Obstet Gynecol. 1984 Jun 15;149(4):450-4. doi: 10.1016/0002-9378(84)90161-3.
Angiotensins I, II, and III, renin substrate, and des-Asp1-angiotensin I were injected as a bolus into either the maternal or fetal circulation of human placental cotyledons perfused in vitro. All drugs tested produced dose-related increments in fetal perfusion pressure when injected into the fetal circulation, with the order of potency being angiotensin I approximately equal to angiotensin II approximately equal to angiotensin III greater than or equal to des-Asp1-angiotensin I greater than or equal to renin substrate. The responses to all the drugs could be blocked by the competitive inhibitor of angiotensin II, (Sar1, Ala8)-angiotensin II, but only the actions of angiotensin I, renin substrate, and des-Asp1-angiotensin I could be blocked by angiotensin converting enzyme inhibitor. When the agents were injected into the maternal circulation, only angiotensins II and III caused dose-related increments in fetal perfusion pressure. Possibly, the placenta may be the main site of conversion of angiotensin I to angiotensin II in the fetoplacental unit, and angiotensin II produced by the placenta could act locally to control fetoplacental blood flow.
将血管紧张素I、II和III、肾素底物以及脱天冬氨酸1 -血管紧张素I作为团注注射到体外灌注的人胎盘小叶的母体或胎儿循环中。当注入胎儿循环时，所有测试药物均使胎儿灌注压产生剂量相关的升高，其效力顺序为血管紧张素I约等于血管紧张素II约等于血管紧张素III大于或等于脱天冬氨酸1 -血管紧张素I大于或等于肾素底物。血管紧张素II的竞争性抑制剂（Sar1，Ala8） - 血管紧张素II可阻断对所有药物的反应，但只有血管紧张素I、肾素底物和脱天冬氨酸1 -血管紧张素I的作用可被血管紧张素转换酶抑制剂阻断。当将这些药物注入母体循环时，只有血管紧张素II和III引起胎儿灌注压的剂量相关升高。胎盘可能是胎儿 - 胎盘单位中血管紧张素I转化为血管紧张素II的主要部位，胎盘产生的血管紧张素II可在局部起作用以控制胎儿 - 胎盘血流。
