Table 1.

Summary of the RAAS in normal pregnancy and pre-eclampsia

Normal pregnancy	Pre-eclampsia
• The RAAS is highly activated in normal pregnancy	• The RAAS is suppressed during the clinical phase of preeclampsia
• The RAAS contributes to plasma volume expansion and vasodilation in pregnancy	• The balance between vasodilatory arm (A1-7) and the vasoconstrictor arm (angiotensin II) favours vasoconstriction
• The balance between vasodilatory arm (A1-7) and the vasoconstrictor arm (angiotensin II) favours vasodilation	• The sensitivity to angiotensin II is increased by AT1-AA and dimerization of the AT1-receptor
• The pressor responsiveness to angiotensin II is reduced by inactivation of the monomeric AT1-receptor	• Components of the local uteroplacental RAAS are upregulated in preeclampsia
• The adrenal responsiveness to angiotensin II is increased and together with non-angiotensin factors contribute to higher aldosterone for the observed renin levels	• Over activation of the AT1-receptor by angiotensin II and/or AT1-AA induces the release of sFlt-1 and other pathogenic factors by the placenta
• The local uteroplacental RAAS is involved in the regulation of trophoblast invasion, angiogenesis and placental blood flow	• Over activation of the AT1-receptor impairs trophoblast invasion, angiogenesis and placental blood flow

RAAS, renin-angiotensin system