The effects of the components of the renin-angiotensin system on the isolated perfused human placental cotyledon.
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.
D000809:Angiotensins / Q000494:pharmacology*; D005260:Female; D005333:Fetus / Q000187:drug effects; D006801:Humans; D009842:Oligopeptides / Q000494:pharmacology; D010920:Placenta / Q000187:drug effects*; D011247:Pregnancy; D011312:Pressure; D012084:Renin-Angiotensin System / Q000187:drug effects*; D013722:Teprotide; D014655:Vascular Resistance / Q000187:drug effects
D000809:Angiotensins; D009842:Oligopeptides; D013722:Teprotide