Effectiveness of nitric oxide agents in preventing the early onset of pre-eclampsia and possible modification of metabolic factors in high-risk pregnancies: a systematic review protocol

Nnate, Daniel A.; Mabhala, Mzwandile A.; Massey, Andrew

doi:10.11124/jbisrir-d-19-00290

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…In contrast, a Cochrane analysis based on randomized trials using NO donors (glyceryl trinitrate) or precursors ( l -arginine), concluded to a lack of reliable conclusions about their efficacy to prevent PE complications [ 226 ]. Finally, a systematic review is currently under investigation, to evaluate published randomized control trials investigating the ability of different NO agents to prevent PE [ 227 ].…”

Section: Therapeutic Perspectives Targeting Oxidative Stress and No/ementioning

confidence: 99%

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

et al. 2021

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Preeclampsia (PE) is a multifactorial pregnancy disease, characterized by new-onset gestational hypertension with (or without) proteinuria or end-organ failure, exclusively observed in humans. It is a leading cause of maternal morbidity affecting 3–7% of pregnant women worldwide. PE pathophysiology could result from abnormal placentation due to a defective trophoblastic invasion and an impaired remodeling of uterine spiral arteries, leading to a poor adaptation of utero-placental circulation. This would be associated with hypoxia/reoxygenation phenomena, oxygen gradient fluctuations, altered antioxidant capacity, oxidative stress, and reduced nitric oxide (NO) bioavailability. This results in part from the reaction of NO with the radical anion superoxide (O 2 •− ), which produces peroxynitrite ONOO - , a powerful pro-oxidant and inflammatory agent. Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S -glutathionylation). The uncoupling of eNOS triggers a switch of its activity from a NO-producing enzyme to a NADPH oxidase-like system generating O 2 •− , thereby potentiating ROS production and oxidative stress. Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production. This review summarizes the dysfunction of placental eNOS evoked by oxidative stress and lipid peroxidation products, and the potential consequences on PE pathogenesis.

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Section: Therapeutic Perspectives Targeting Oxidative Stress and No/ementioning

confidence: 99%

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

et al. 2021

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“…NO donors have potent vasodilator effect and have been shown to improve blood flow in the fetoplacental circulation during mild preeclampsia [ 126 ]. The vasodilator effect of NO signaling is modulated by the interaction between NO and heme-containing proteins, most notably soluble guanylyl cyclase (sGC) [ 127 ].…”

Section: Hypertensive Disorders Of Pregnancy and Vascular Functionmentioning

confidence: 99%

Dietary supplements and vascular function in hypertensive disorders of pregnancy

Man

Zhou

Xia

et al. 2023

Pflugers Arch - Eur J Physiol

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Hypertensive disorders of pregnancy are complications that can lead to maternal and infant mortality and morbidity. Hypertensive disorders of pregnancy are generally defined as hypertension and may be accompanied by other end organ damages including proteinuria, maternal organ disturbances including renal insufficiency, neurological complications, thrombocytopenia, impaired liver function, or uteroplacental dysfunction such as fetal growth restriction and stillbirth. Although the causes of these hypertensive disorders of pregnancy are multifactorial and elusive, they seem to share some common vascular-related mechanisms, including diseased spiral arteries, placental ischemia, and endothelial dysfunction. Recently, preeclampsia is being considered as a vascular disorder. Unfortunately, due to the complex etiology of preeclampsia and safety concerns on drug usage during pregnancy, there is still no effective pharmacological treatments available for preeclampsia yet. An emerging area of interest in this research field is the potential beneficial effects of dietary intervention on reducing the risk of preeclampsia. Recent studies have been focused on the association between deficiencies or excesses of some nutrients and complications during pregnancy, fetal growth and development, and later risk of cardiovascular and metabolic diseases in the offspring. In this review, we discuss the involvement of placental vascular dysfunction in preeclampsia. We summarize the current understanding of the association between abnormal placentation and preeclampsia in a vascular perspective. Finally, we evaluate several studied dietary supplementations to prevent and reduce the risk of preeclampsia, targeting placental vascular development and function, leading to improved pregnancy and postnatal outcomes.

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“…Reduction of nitric oxide bioavailability may contribute to vascular dysfunction in preeclampsia ( 26 , 27 ). Consequently, nitric oxide donors are being considered potential candidates to examine for the treatment of preeclampsia ( 28 , 29 ).…”

Section: Introductionmentioning

confidence: 99%

The L-NAME mouse model of preeclampsia and impact to long-term maternal cardiovascular health

et al. 2022

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Preeclampsia affects ∼2–8% of pregnancies worldwide. It is associated with increased long-term maternal cardiovascular disease risk. This study assesses the effect of the vasoconstrictor N(ω)-nitro-L-arginine methyl ester (L-NAME) in modelling preeclampsia in mice, and its long-term effects on maternal cardiovascular health. In this study, we found that L-NAME administration mimicked key characteristics of preeclampsia, including elevated blood pressure, impaired fetal and placental growth, and increased circulating endothelin-1 (vasoconstrictor), soluble fms-like tyrosine kinase-1 (anti-angiogenic factor), and C-reactive protein (inflammatory marker). Post-delivery, mice that received L-NAME in pregnancy recovered, with no discernible changes in measured cardiovascular indices at 1-, 2-, and 4-wk post-delivery, compared with matched controls. At 10-wk post-delivery, arteries collected from the L-NAME mice constricted significantly more to phenylephrine than controls. In addition, these mice had increased kidney Mmp9:Timp1 and heart Tnf mRNA expression, indicating increased inflammation. These findings suggest that though administration of L-NAME in mice certainly models key characteristics of preeclampsia during pregnancy, it does not appear to model the adverse increase in cardiovascular disease risk seen in individuals after preeclampsia.

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Effectiveness of nitric oxide agents in preventing the early onset of pre-eclampsia and possible modification of metabolic factors in high-risk pregnancies: a systematic review protocol

Cited by 4 publications

References 19 publications

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

Role of oxidative stress in the dysfunction of the placental endothelial nitric oxide synthase in preeclampsia

Dietary supplements and vascular function in hypertensive disorders of pregnancy

The L-NAME mouse model of preeclampsia and impact to long-term maternal cardiovascular health

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