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The etiology of pregnancy-induced hypertension based on the degradation of angiotensin II by placental aminopeptidases

基于胎盘氨肽酶降解血管紧张素 II 的妊娠高血压病因

基本信息

批准号：
61570787
负责人：
MIZUTANI Shigehiko
金额：
$ 1.47万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1988
项目状态：
已结题

项目摘要

(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.

(1)我们目前的研究表明，血管紧张素降解是由于氨肽酶A和M在人胎盘，氨肽酶A和P-β-氨基肽酶在妊娠血清中，分别。(2)妊娠与对外源性血管紧张素II（A-II）升压作用的难治性反应有关;然而，妊娠高血压（PIH）患者和非妊娠妇女对A-II的作用敏感。我们的研究表明，妊娠期对A-II无效是由于胎盘氨肽酶A和M的失活增加。(3)我们检测了PIN患者母亲外周血管紧张素I（A-I）、血管紧张素转换酶（ACE）和血管紧张素酶（氨肽酶A，P-ACE）水平。妊高征组A-I、ACE水平与正常妊娠组相似。妊高征组氨肽酶A和P-β活力明显低于正常妊娠组。本研究提示血管紧张素酶可能参与妊高征的发病。