Nitric Oxide Signaling in Preeclampsia Management
Summary
Preeclampsia remains a leading cause of maternal and perinatal morbidity and mortality worldwide, characterised by new-onset hypertension and organ dysfunction after 20 weeks’ gestation. Central to its pathophysiology is impaired production and bioavailability of nitric oxide (NO), a gaseous vasodilator synthesised by endothelial NO synthase from L-arginine. In healthy pregnancy, NO promotes uteroplacental blood flow, supports trophoblast invasion and maintains endothelial homeostasis. In preeclampsia, elevated levels of endogenous NOS inhibitors such as asymmetric dimethylarginine (ADMA), oxidative stress and inflammatory mediators converge to reduce NO synthesis, precipitating vasoconstriction, placental hypoperfusion and systemic endothelial dysfunction. Restoration of NO signalling through dietary nitrate, NO donors, L-arginine supplementation or phosphodiesterase inhibitors has shown promise in ameliorating blood pressure and improving placental perfusion. Genetic and epigenetic regulation of key enzymes, including dimethylarginine dimethylaminohydrolase (DDAH) isoforms responsible for ADMA clearance, further modulates individual risk and therapeutic responsiveness. A nuanced understanding of these pathways has enabled the development of predictive biomarkers, stratification of patient subgroups and exploration of targeted interventions that aim to restore vascular resilience, reduce maternal cardiovascular burden and improve perinatal outcomes.
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Nitric Oxide Signaling in Preeclampsia Management publication trend
The graph below shows the total number of articles in nitric oxide signaling in preeclampsia management across all publications each year (not limited to Nature Index journals).
Technical terms
Nitric oxide (NO): A gaseous signalling molecule produced by endothelial NO synthase that relaxes vascular smooth muscle via cGMP synthesis.
Asymmetric dimethylarginine (ADMA): An endogenous NOS inhibitor that competes with L-arginine, reducing NO production and promoting endothelial dysfunction.
L-arginine: A semi-essential amino acid and substrate for NO synthase, supplementation of which can enhance NO availability.
Endothelial dysfunction: A state of impaired vasodilation, pro-inflammatory and pro-thrombotic activity that underlies the vascular pathology of preeclampsia.
DDAH2: Dimethylarginine dimethylaminohydrolase isoform 2, the enzyme responsible for metabolising ADMA and maintaining NO homeostasis.
References
- The Role of Nitric Oxide, ADMA, and Homocysteine in The Etiopathogenesis of Preeclampsia—Review. International Journal of Molecular Sciences (2019).
- Cellular signaling with nitric oxide and cyclic GMP. Brazilian Journal of Medical and Biological Research (1999).
- Early and late-onset preeclampsia: effects of DDAH2 polymorphisms on ADMA levels and association with DDAH2 haplotypes. Revista Brasileira de Ginecologia e Obstetrícia (2024).
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