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)的升压效应有关；然而，妊娠高血压综合征(PIH)患者和非妊娠妇女对A-II的作用敏感。我们的研究表明，妊娠期间对A-II的这种难治性是由于胎盘氨肽酶A和M的失活增加所致。(3)我们测定了PIN患者母体外周血管紧张素转换酶(ACE)和血管紧张素酶(氨基肽酶A，P-LAP)的水平。妊高征组A-I和ACE水平与正常妊娠组相近。而妊高征组的氨基肽酶A和P-LAP活性均显着低于正常妊娠组。我们目前的研究表明血管紧张素可能参与了妊高征发病。

(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.