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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.
T Hosokawa, and
R B Howard, and
M H Maguire
December 1998,
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T Hosokawa, and
R B Howard, and
M H Maguire
May 1971,
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T Hosokawa, and
R B Howard, and
M H Maguire
May 1976,
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T Hosokawa, and
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M H Maguire
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T Hosokawa, and
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T Hosokawa, and
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M H Maguire
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T Hosokawa, and
R B Howard, and
M H Maguire
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T Hosokawa, and
R B Howard, and
M H Maguire
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T Hosokawa, and
R B Howard, and
M H Maguire
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T Hosokawa, and
R B Howard, and
M H Maguire
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