Key result
Hypertensive pregnancies are linked to stalled RAAS activation and lower third-trimester aldosterone.
Why the study?
Hypertension during pregnancy increases adverse maternal and fetal risks, but the underlying mechanisms and characteristics of renin-angiotensin-aldosterone system alterations remain incompletely understood.
Are RAAS peptide and effector profiles altered over gestation in pregnant women who develop gestational hypertension and pre-eclampsia compared to those who remain normotensive?
Cohort (n=74)
Are RAAS peptide and effector profiles altered over gestation in pregnant women who develop gestational hypertension and pre-eclampsia compared to those who remain normotensive?
Pregnancies complicated by hypertension or pre-eclampsia are characterized by an attenuated activation of the renin-angiotensin-aldosterone system in the second half of pregnancy compared to normotensive pregnancies.
May aid risk stratification in hypertensive pregnancies; leaves open whether RAAS modulation alters outcomes.
Hypertension during pregnancy increases the risk of adverse maternal and fetal outcomes, but the mechanisms of pregnancy hypertension are not precisely understood. Elevated plasma renin activity and aldosterone concentrations play an important role in the normal physiologic adaptation to pregnancy. These effectors are reduced in patients with pregnancy hypertension, creating an opportunity to define the features of the renin-angiotensin-aldosterone system (RAAS) that are characteristic of this disorder. In the current study, we used a novel LC-MS/MS-based methodology to develop comprehensive profiles of RAAS peptides and effectors over gestation in a cohort of 74 pregnant women followed prospectively for the development of gestational hypertension and pre-eclampsia (HYP, 27 patients) versus those remaining normotensive (NT, 47 patients). In NT pregnancy, the plasma renin activity surrogate, (PRA-S, calculated from the sum of Angiotensin I + Angiotensin II) and aldosterone concentrations significantly increased from the first to the third trimester, accompanied by a modest increase in the concentrations of angiotensin peptide metabolites. In contrast, in HYP pregnancies, PRA-S and angiotensin peptides were largely unchanged over gestation, and third-trimester aldosterone concentrations were significantly lower compared with those in NT pregnancies. The results indicated that the predominant features of pregnancies that develop HYP are stalled or waning activation of the RAAS in the second half of pregnancy (accompanied by unchanging levels of angiotensin peptides) and the attenuated secretion of aldosterone.
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Shoemaker et al. (2023) conducted a cohort in Pregnancy hypertension (gestational hypertension and pre-eclampsia) (n=74). Development of gestational hypertension and pre-eclampsia (HYP) vs. Remaining normotensive (NT) was evaluated on Comprehensive profiles of RAAS peptides and effectors (PRA-S and aldosterone concentrations). Pregnancies developing hypertension showed stalled RAAS activation and significantly lower third-trimester aldosterone concentrations compared with normotensive pregnancies.
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