Conversion of angiotensin I to angiotensin II in the human foetoplacental vascular bed.
Pressor effects of angiotensin I (AI) and angiotensin II (AII) on the human foetoplacental vasculature were compared in dual-perfused term placental cotyledons in which foetoplacental perfusion pressure was monitored. Arterial injections of 1 nmol doses of AI and AII caused marked increases in perfusion pressure; the mean pressor response to AI was 92.9 +/- 5.8% (mean +/- s.e. mean) of the AII response. The angiotensin-converting enzyme inhibitor captopril at 2.2 microM reversibly reduced the AI response to 13.7 +/- 3.2% (mean +/- s.e. mean) of the AII response, which was unaffected. Saralasin, an AII receptor blocker, at 94 nM reversibly antagonized both AI-and AII-induced increases in foetoplacental perfusion pressure. It is concluded that foetoplacental vasoconstriction elicited by AI is due to its conversion to AII by angiotensin-converting enzyme present in the foetoplacental bed.
D000803:Angiotensin I / Q000378:metabolism* / Q000494:pharmacology; D000804:Angiotensin II / Q000378:metabolism* / Q000494:pharmacology; D000809:Angiotensins / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D010920:Placenta / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D012504:Saralasin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects*
D000809:Angiotensins; D000804:Angiotensin II; D000803:Angiotensin I; D002216:Captopril; D012504:Saralasin