Journal
CURRENT VASCULAR PHARMACOLOGY
Volume 14, Issue 3, Pages 237-259Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570161114666160222115158
Keywords
Preeclampsia; diabetes; hypercholesterolaemia; nitric oxide; endothelium; fetoplacental
Funding
- Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT), Chile [1150344, 1150377, 3130583, 3140516]
- Faculty of Medicine, PUC-PhD fellowships
- Vicerectorate of Research, PUC-PhD fellowship
- Comision Nacional de Investigacion en Ciencia y Tecnologia (CONICYT)-PhD fellowships
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Preeclampsia (PE), gestational diabetes mellitus (GDM), and maternal supraphysiological hypercholesterolaemia (MSPH) are pregnancy-related conditions that cause metabolic disruptions leading to alterations of the mother, fetus and neonate health. These syndromes result in fetoplacental vascular dysfunction, where nitric oxide (NO) plays a crucial role. PE characterizes by abnormal increase in the placental blood pressure and a negative correlation between NO level and fetal weight, suggesting that increased NO level and oxidative stress could be involved. GDM courses with macrosomia along with altered function of the fetal cardiovascular system and fetoplacental vasculature. Even when NO synthesis in the fetoplacental vasculature is increased, NO bioavailability is reduced due to the higher oxidative stress seen in this disease. In MSPH, there is an early development of atherosclerotic lesions in fetal and newborn arteries, altered function of the fetoplacental vasculature, and higher markers of oxidative stress in fetal blood and placenta, thus, vascular alterations related with NO metabolism occur as a consequence of this syndrome. Potential mechanisms of altered NO synthesis and bioavailability result from transcriptional and post-translational NO synthases (NOS) modulation, including phosphorylation/dephosphorylation cycles, coupling/uncoupling of NOS, tetrahydrobiopterin bioavailability, calcium/calmodulin-NOS and caveolin-1-NOS interaction. Additionally, oxidative stress also plays a role in the reduced NO bioavailability. This review summarizes the available information regarding lower NO bioavailability in these pregnancy pathologies. A common NO-dependent mechanism in PE, GDM and MSPH contributing to fetoplacental endothelial dysfunction is described.
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