Nitric oxide is a central common metabolite in vascular dysfunction associated with diseases of human pregnancy

Leiva, Andrea, Fuenzalida, Barbara, Barros, Eric, Sobrevia, Bastian, Salsoso, Rocio, Saez, Tamara, Villalobos, Roberto, Silva, Luis, Chiarello, Indira, Toledo, Fernando, Gutierrez, Jaime, Sanhueza, Carlos, Pardo, Fabian and Sobrevia, Luis (2016) Nitric oxide is a central common metabolite in vascular dysfunction associated with diseases of human pregnancy. Current Vascular Pharmacology, 14 3: 237-259. doi:10.2174/1570161114666160222115158


Author Leiva, Andrea
Fuenzalida, Barbara
Barros, Eric
Sobrevia, Bastian
Salsoso, Rocio
Saez, Tamara
Villalobos, Roberto
Silva, Luis
Chiarello, Indira
Toledo, Fernando
Gutierrez, Jaime
Sanhueza, Carlos
Pardo, Fabian
Sobrevia, Luis
Title Nitric oxide is a central common metabolite in vascular dysfunction associated with diseases of human pregnancy
Journal name Current Vascular Pharmacology   Check publisher's open access policy
ISSN 1570-1611
1875-6212
Publication date 2016-01-01
Sub-type Article (original research)
DOI 10.2174/1570161114666160222115158
Open Access Status Not yet assessed
Volume 14
Issue 3
Start page 237
End page 259
Total pages 23
Place of publication Bussum, Netherlands
Publisher Bentham Science Publishers
Language eng
Abstract 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.
Keyword Preeclampsia
Diabetes
Hypercholesterolaemia
Nitric oxide
Endothelium
Fetoplacental
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
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