Abstract

[Figure: see text].

Highlights

  • Various studies found an association of different renin-angiotensin system (RAS) components with gestational duration and preterm birth, as well as with preeclampsia

  • Lower placental leucinyl aminopeptidase (LNPEP) in PE and in early gestation higher-risk patients implicates a new alternative RAS mechanism contributing to hypertension in pregnancy

  • We further investigated the expression of Ang-converting enzymes REN, ACE, ACE2, ENPEP, Aminopeptidase N (ANPEP), RNPEP, DPP3 (Figure S1, modified from19), which were partially present in the placenta to convert exogenous Ang depending on cell type (Figure 1A)

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Summary

Introduction

Various studies found an association of different renin-angiotensin system (RAS) components with gestational duration and preterm birth, as well as with preeclampsia. Lower placental LNPEP in preeclampsia and in first-trimester patients at high-risk for preeclampsia suggests a new alternative route in maternal RAS signaling and may contribute to hypertension and disease in pregnancy. 25% of firsttime pregnant women develop a mild to severe hypertension in pregnancy or even preeclampsia[1] and 37% develop elevated blood pressure but not overt hypertension.[2] Women diagnosed with gestational hypertension experience increased morbidity, including augmented rates of caesarean deliveries, abruptio placentae, and acute renal dysfunction.[1] Depending on the country of origin, 10% to 50% of women initially diagnosed with gestational hypertension end up developing preeclampsia in as short a period as 1 to 5 weeks.[3,4] chronic hypertension ranks second in risk factors for women developing preeclampsia (16%).[5]. Leptin downregulates placental LNPEP. Preeclamptic placentae and placentae from an early gestation high-risk population have decreased LNPEP compared with controls

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