ESA-SRB-AOTA 2019

Angiotensin converting enzyme 2 (ACE2) and pregnancy complications: preeclampsia and small for gestational age. (#140)

Sonia Tamanna 1 2 3 , Vicki L. Clifton 4 5 , Kym Rae 1 6 7 , Dirk Van Helden 2 , Eugenie R. Lumbers 1 2 3 , Kirsty G. Pringle 1 2 3
  1. Pregnancy and Reproduction Program, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia
  2. School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia
  3. Priority Research Centre for Reproductive Sciences, University of Newcastle , Newcastle, New South Wales, Australia
  4. MaterMedical Research Institute and Translational Research Institute, University of Queensland , Brisbane, QLD, Australia
  5. Australia Robinson Research Institute, School of Medicine, University of Adelaide , Adelaide, SA, Australia
  6. Department of Rural Health, University of Newcastle, Tamworth, Newcastle, NSW , Australia
  7. Priority Research Centre for Generational Health and Ageing, University of Newcastle, Newcastle, NSW, Australia

Preeclampsia (PE) and small for gestational age (SGA) are common pregnancy complications and remain a major health burden to both mother and fetus. Nevertheless, the pathophysiological causes of PE and SGA are not very well understood or documented. Therefore, early detection and identification of precise blood biomarkers are required to treat these diseases better. During pregnancy, the renin-angiotensin system (RAS) plays significant roles in the regulation of blood pressure. An imbalance in the RAS peptides may contribute to the pathophysiology of PE and SGA. We aimed to examine maternal levels of angiotensin (Ang) peptides and enzymes across gestation and in PE and SGA pregnancies. Plasma samples were collected from non-pregnant women (n=10) as well as from women with uncomplicated pregnancies (n=80), SGA (n=25) or PE (n=14) across gestation (13-36 weeks). Angiotensin converting enzyme (ACE) and ACE2 levels were measured by ELISA, Ang II and Ang-(1-7) were measured by RIA. Plasma ACE and ACE2 levels were significantly higher in healthy pregnant women compared with non-pregnant women (p<0.05) and remained high throughout gestation. Conversely, Ang II was decreased and Ang-(1-7) increased in pregnant women compared with non-pregnant women, thus Ang II/Ang-(1-7) was decreased. Women with SGA had levels of ACE, Ang II and Ang-(1-7) that were similar to healthy pregnant women but ACE2 levels were reduced (p<0.005). In women with PE, ACE levels were decreased compared to healthy pregnant women (p<0.003) but Ang II levels were increased (P<0.003). These studies show for the first time that plasma ACE2 levels increase in pregnancy. Therefore, ACE2 is likely playing a role in producing Ang-(1-7), thus stimulating the vasodilatory RAS pathway in pregnancy. Women with PE have decreased plasma ACE levels but increased Ang II suggesting that other enzymes (e.g. chymase) are producing Ang II in women with PE.