Abstract
IntroductionAn imbalance in angiotensin (Ang) peptides could contribute to the pathophysiology of preeclampsia (PE) and poor fetal growth.MethodsWe measured maternal plasma levels of Ang peptides and converting enzymes in non-pregnant women (n = 10), in normal pregnant women (n = 59), women delivering small for gestational age babies (SGA, n = 25) across gestation (13–36 weeks) and in women with PE (n = 14) in their third trimester.ResultsPlasma ACE, ACE2, and Ang-(1-7) levels, and ACE2 activity were significantly higher in normal pregnant women compared with non-pregnant women; neprilysin (NEP) levels were not changed. In SGA pregnancies, ACE and ACE2 levels were higher in early-mid pregnancy compared with normal pregnant women. In women with PE, plasma ACE, ACE2, NEP, and Ang-(1-7) levels and ACE2 activity were lower than levels in normal pregnant women.ConclusionThe higher plasma ACE2 levels and activity in pregnancy could be driving the higher Ang-(1-7) levels. The early gestation increases in ACE and ACE2 levels in SGA pregnancies highlights the possibility that these enzymes could be used as potential early biomarkers of poor fetal growth. In women with PE, the reduced ACE2 and NEP levels at term, could be contributing to the reduction in Ang-(1-7) levels. These findings suggest that dysfunctional relationships between two key enzymes in the circulating RAS are involved in the pathogenesis of PE and SGA. Since soluble ACE2 can prevent binding of the novel coronavirus, SARS-CoV-2, to membrane bound ACE2, the interplay between ACE2 and the coronavirus and its impact in pregnancy requires further investigation.
Highlights
An imbalance in angiotensin (Ang) peptides could contribute to the pathophysiology of preeclampsia (PE) and poor fetal growth
Data and biobanked plasma samples from a cohort study undertaken at the Lyell McEwin Hospital, Adelaide, Australia, that was used to study the effects of asthma during pregnancy on the mother, placenta and baby, were examined (Dickinson et al, 2016)
We showed for the first time that angiotensin converting enzyme (ACE) and ACE2 levels and activity were increased in the maternal circulation during pregnancy and remained high throughout gestation, NEP levels were unchanged
Summary
An imbalance in angiotensin (Ang) peptides could contribute to the pathophysiology of preeclampsia (PE) and poor fetal growth. The renin-angiotensin system (RAS) plays a significant role in the regulation of blood pressure and salt and water balance. It is activated by estrogen-induced increases in angiotensinogen (AGT) and, subsequently, by the reduction in systemic vascular resistance caused by the ovarian hormone, relaxin (Lumbers and Pringle, 2014). The circulating RAS cascade (Figure 1) begins with the release of active renin from the kidney, which cleaves angiotensin I (Ang I) from AGT. Interactions between Ang II and the AT1R stimulate sodium retention (both directly and via stimulating the release of aldosterone) and raise blood pressure, both by central actions and direct effects on blood vessels. Ang II can bind to the AT2R, which has opposing actions than those of Ang II binding to the AT1R (Escobar et al, 2004)
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