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Placenta may exert fetal protection against maternal high salt diet intake via renin-angiotensin-aldosterone system.
- Source :
- Placenta; Dec2024, Vol. 158, p136-144, 9p
- Publication Year :
- 2024
-
Abstract
- This study investigated the effects of high compared to normal dietary salt intake on fetoplacental vascular function, activity of renin-angiotensin-aldosterone system (RAAS), placental pro- and anti-angiogenic factors and biomarkers of placental remodeling and oxidative stress during healthy uncomplicated pregnancy. Based on their 24-h sodium excretion pregnant women (37–40 weeks' gestation) were categorized into three groups: normal salt (NS, <5.75 g/day, N = 12), high salt (HS, 5.75–10.25 g/day, N = 36), and very high salt (VHS, >10.25 g/day, N = 17). Pulsatility (PI) and resistive index of middle cerebral artery (MCA) and umbilical artery, plasma renin activity (PRA), serum aldosterone, soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) concentrations, as well as placental vascular endothelial growth factor C (VEGF-C), oxidative/antioxidative stress markers (TBARS/FRAP) and matrix metalloproteinase 9 (MMP-9) concentration were measured. PI MCA was significantly decreased in HS/VHS groups compared to NS group. HS/VHS intake did not suppress PRA and aldosterone concentration. Serum PlGF concentration was significantly increased while sFlt-1 concentration and sFlt-1/PlGF ratio were significantly decreased in VHS group compared to NS group. MMP-9, VEGF-C concentration, TBARS and FRAP in placental tissue were similar between study groups. HS/VHS diet does not suppress RAAS during pregnancy; however, it is associated with decreased PI MCA, a significantly decreased sFlt-1/PlGF ratio and unchanged biomarkers of placental remodeling or oxidative stress in healthy pregnant women, suggesting the presence of a possible protective or compensatory mechanism aimed at preserving placental function and pregnancy outcome itself in terms of maternal HS intake. • High-salt diet (HSD) during pregnancy affects maternal endothelial function. • However, HSD is not associated with adverse pregnancy outcome. • RAAS activity is maintained and sFlt1/PlGF reduced with HSD during pregnancy. • Biomarkers of placental remodeling and oxidative stress are not affected by maternal HSD. • Some protective or compensatory mechanisms preserve placental function during HSD. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 01434004
- Volume :
- 158
- Database :
- Supplemental Index
- Journal :
- Placenta
- Publication Type :
- Academic Journal
- Accession number :
- 181494012
- Full Text :
- https://doi.org/10.1016/j.placenta.2024.10.003