Abstract
Nitric oxide (NO) regulates placental blood flow and actively participates in trophoblast invasion and placental development. Asymmetric dimethylarginine (ADMA) can inhibit NO synthase, which generates NO. ADMA has been associated with uterine artery flow disturbances such as preeclampsia. Substantial experimental evidence has reliably supported the hypothesis that an adverse in utero environment plays a role in postnatal physiological and pathophysiological programming. Growing evidence suggests that the placental nitrergic system is involved in epigenetic fetal programming. In this review, we discuss the roles of NO and ADMA in normal and compromised pregnancies as well as the link between placental insufficiency and epigenetic fetal programming.
Highlights
Nitric oxide (NO), the main vasodilator in the placenta, is involved in the regulation of feto-placental vascular reactivity, placental bed vascular resistance, trophoblast invasion and apoptosis, and platelet adhesion and aggregation in the intervillous space [1,2,3]
Maternal plasma Asymmetric dimethylarginine (ADMA) levels are reduced in a normal pregnancy but increase as the gestational age increases [9,10] and is increased in compromised pregnancies such as those with preeclampsia [9,10]
Placental nutrient transport is dependent on vascular development; NO plays a critical role
Summary
Nitric oxide (NO), the main vasodilator in the placenta, is involved in the regulation of feto-placental vascular reactivity, placental bed vascular resistance, trophoblast invasion and apoptosis, and platelet adhesion and aggregation in the intervillous space [1,2,3]. Placental vascular development is a crucial process required for adequate fetal development [1,4]. Placenta insufficiencies such as in gestational diabetes mellitus (GDM), intrauterine growth restriction (IUGR), and preeclampsia are related to vascular dysfunction of the placenta [5]. The placenta plays a central role in fetal programming by directly regulating blood flow, transporter activity, fetal nutrient supply and fetal growth [11,12]. It has been suggested that therapeutic agents, which target placental blood flow and vascular development, ameliorate fetal growth restriction [2,5]. Manipulation of the ADMA-NO pathways may have a therapeutic potential to rescue placental blood flow and improve long-term outcomes in patients with placental insufficiencies
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