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Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health, 2015

Abstract

A vasodilator pathway of the RAAS has been described, including the angiotensin converting enzyme 2 (ACE2) and the vasodilator Ang(1-7). The pressor effects of Angiotensin-II (Ang-II) are reduced in normal pregnancy, and partially restored in pre-eclampsia. To examine activity of the ACE2/Ang(1-7) axis of the RAAS in normal and hypertensive pregnancy. Women in their 3rd trimester and non-pregnant women had measurement of plasma Renin concentration (PRC), Aldosterone (PAC), ACE1 & ACE2, Angiotensin II (AII) and Ang(1-7) in a cross sectional study. There were five groups: normotensive pregnancy (NP, n= 16); gestational hypertension (GH, n= 40); essential hypertension (EH, n= 9), pre-eclampsia (PE, n= 7) and non-pregnant controls (C, n=23). (1) PRC was higher in NP-30mU/L than C-19mU/L, EH-19mU/L and PE-17mU/L (p<0.05) but women with GH had similar levels to normal pregnancy (26U/L). (2) Aldosterone concentration was higher in NP-1715pmol/L compared to C-471pmol/L (p<0.001) and compared to all hypertensive groups (GH-1287, EH-881 and PE-817pmol/L), p<0.05. (3) Aldo/renin ratios did not differ amongst groups (C-26, NP-71, EH-38, GH-69, PE-77). (4) ACE2 concentrations were higher in NP-276mU/L than C-119mU/L (p<0.001), but similar to that in hypertensive pregnancies (GH-305, EH-296, PE-332mU/L). (5) Plasma angiotensin II was higher in NP-114pg/ml than C-56pg/ml (p<0.001) but also similar to that in hypertensive pregnancies (GH-121pg/ml, EH-92pg/ml, PE-89pg/ml). (6) Neither Ang(1-7) nor ACE1 levels differed amongst groups. In normal pregnancy, as expected, PRC, PAC and AII are increased, so too is the ACE2 enzyme but without an accompanying increase in A1-7, perhaps a type 2 error or perhaps implying other physiological control of A1-7 production. In pre-eclampsia and EH there were consistent falls in PRC and PAC without a change in either ACE2 or A1-7 which may represent a compensatory shift in balance of the RAAS towards vasodilatation. F.M. Pettit: None. J. Spaan: None. G.J. Mangos: None. G. Davis: None. A. Henry: None. M.A. Brown: None.

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