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

(1)我们目前的研究表明，血管紧张素的降解是由于人胎盘中的氨基肽酶A和M，以及妊娠血清中的氨基肽酶A和P-LAP。(2)妊娠与外源性血管紧张素II（a -II）升压作用的难治性反应有关；而妊高征（PIH）患者和非孕妇对A-II的影响较为敏感。我们的研究表明，妊娠期对A- ii的难治性是由于胎盘氨肽酶A和m的失活增加。(3)我们测量了PIN患者母体外周血管紧张素I-(A-I)、血管紧张素转换酶（ACE）和血管紧张酶（氨肽酶A， P-LAP）水平。妊高征患者A-I和ACE水平与正常妊娠相似。而妊高围组氨肽酶A和P-LAP活性明显低于正常妊娠组。我们目前的研究表明血管紧张素可能参与PIH的发病。

(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.