1988 Fiscal Year Final Research Report Summary
The etiology of pregnancy-induced hypertension based on the degradation of angiotensin II by placental aminopeptidases
| Project/Area Number |
61570787
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nagoya University |
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Principal Investigator |
MIZUTANI Shigehiko Nagoya University School of Medicine, 医学部, 助教授 (00159162)
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| Co-Investigator(Kenkyū-buntansha) |
KASUGAI Masahide Nagoya University School of Medicine, 医学部, 助手 (00185787)
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| Project Period (FY) |
1986 – 1988
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| Keywords | Angiotensinase / Placental aminopeptidase / Refractoriness to angiotensin II / Pregnancy-induced hypertension / Treatment of pregnancy-induced hypertension / Angiotensin II receptor / 遺伝子工学 |
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| Research Abstract |
(1) Our present study showed that angiotensin degradation is due to aminopeptidases A and M in the human placenta, and to aminopeptidase A and P-LAP in pregnancy serum, respectively.
(2) Pregnancy is associated with a refractory response to the pressor effect of exogenously infused angiotensin II(A-II); patients with pregnancy-induced hypertension (PIH) and non-pregnant women, however, are sensitive to the effect of A-II. Our study suggested that such refractoriness to A-II in pregnancy is due to increased inactivation by placental aminopeptidases A and M.
(3) We measeued maternal peripheral angiotensin I-(A-I) and angitensin-converting enzyme(ACE) and angiotensinases(aminopeptidase A, P-LAP) levels in patients with PIN. A-I and ACE levels in PIH were similar to those in normal pregnancy. However aminopeptidase A and P-LAP activities in PIH were significantly lower than those in normal pregnancy. Our present study showed the possible involvement of angiotensinaes in the onset of PIH.
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