Reduced l-arginine Level and Decreased Placental eNOS Activity in Preeclampsia

Kim, Y.J.; Park, Hyesook; Lee, H.Y.; Ha, Eun Hee; Suh, Seong-Il; Oh, Se-Hyun; Yoo, Hyun-jung

doi:10.1016/j.placenta.2005.04.011

Cited by 104 publications

(64 citation statements)

References 28 publications

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“…Median maternal concentrations of L-arginine, ADMA, and SDMA were higher (16,13, and 30%, respectively), whereas the maternal ADMA/ SDMA ratio was 12% lower in the preeclampsia group compared with the uncomplicated pregnancy group. There was no statistically significant difference in the maternal L-arginine/ ADMA ratio between preeclampsia patients and controls.…”

Section: Resultsmentioning

confidence: 85%

“…There have been discrepant findings of elevated (15) and unchanged (16,17) ADMA concentrations in the maternal circulation in women with preeclampsia compared with women with uncomplicated pregnancies. Elevated maternal ADMA concentrations have been found preceding the clinical symptoms of preeclampsia (18,19) suggesting that ADMA could have a role in the pathogenesis of preeclampsia.…”

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confidence: 95%

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Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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Preeclampsia is a leading cause of intrauterine growth restriction and preterm birth. Endothelial dysfunction is the common final pathway leading to clinical signs of preeclampsia including hypertension and proteinuria. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The purpose of this study was to investigate maternal and fetal concentrations of ADMA, L-arginine, and symmetric dimethylarginine (SDMA). Women with preeclampsia (n ϭ 47) and controls (n ϭ 51) who gave birth by cesarean section were included in the study. We analyzed the maternal plasma and umbilical vein and artery plasma. We found that not only maternal concentrations of ADMA and SDMA but also L-arginine were significantly higher in women with preeclampsia than in controls. In fetal samples, only SDMA concentrations were higher in the preeclampsia group than in controls. The median ADMA concentration was three times higher in the fetal circulation than in the maternal circulation, but there was no difference between the preeclampsia group and the control group, and the veno-arterious gradient indicated that the placenta was the source of ADMA. (Pediatr Res 66: 411-415, 2009) P reeclampsia is a common pregnancy complication associated with increased risk of preterm birth and fetal growth restriction (1). The exact etiology of preeclampsia is not known, and hence no definitive preventative measures or treatments are available.Endothelial dysfunction is the common final pathway leading to the clinical signs of preeclampsia including hypertension and proteinuria. It is not known to what extent endothelial dysfunction also affects the infant. Increased concentrations of biomarkers for preeclampsia in the maternal circulation are usually not reflected in the infant. Previously, our group has shown that newborns from preeclamptic pregnancies did not differ from those born after uncomplicated pregnancies with respect to circulating biomarkers of inflammation (CRP and calprotectin) (2), and oxidative stress (3), but newborns from preeclamptic pregnancies had elevated concentrations of homocysteine (4).In women with previous preeclampsia, there is an increased risk for cardiovascular disease later in life (5) and an increased risk of hypertension has also been found for their offspring (6,7).It is not clear whether the increased risk in the offspring is caused by the intrauterine environment, shared genes, or impaired intrauterine growth. In epidemiologic and animal studies, low birth weight by itself is associated with an increased risk of cardiovascular disease and metabolic syndrome (8).NO is essential for vascular tone and endothelial function, and elevated circulating concentrations of asymmetric dimethylarginine (ADMA) are associated with reduced vasodilation and endothelial dysfunction (9). ADMA is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The ratio...

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Section: Resultsmentioning

confidence: 85%

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confidence: 95%

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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“…1 It is suggested that the placenta takes a major role in the development of preeclampsia, which, for several proposed reasons, releases factors into the maternal circulation that leads to maternal endothelial dysfunction. 2 Endothelial dysfunction is considered to underlie clinical preeclampsia manifestations, such as maternal hypertension, proteinuria, and edema. 3 Since endothelium is an integral part of the inflammatory network, activated endothelium activates leukocytes and vice versa.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress and inflammatory markers in normal pregnancy and preeclampsia

Bernardi

Guolo

Bortolin

et al. 2008

J of Obstet and Gynaecol

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Aim: Although previous investigators have demonstrated the presence of oxidative stress and inflammation in preeclampsia, none directly correlate both to preeclampsia. Methods: We determined in 35 preeclamptic and 35 normotensive pregnant women plasma levels of thiobarbituric acid reactive species, protein carbonyl, tumour necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6 and IL-10. Results: Plasma thiobarbituric acid reactive species and protein carbonyls were higher in preeclamptic patients. TNF-a and IL-6 (but not IL-1b or IL-10) were higher in preeclamptic patients. We found significant correlation between plasma IL-6 and carbonyls, and these correlated to blood pressure. Conclusions: We demonstrated that some oxidative and inflammatory mediators were altered in preeclampsia, and some correlated to blood pressure.

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“…The concentration of NO in the fetoplacental system depends on many factors including l-arginine availability, the activity levels of NO synthase isoforms, the presence of endogenous NO synthase inhibitors, and species-dependent variation. While some studies have reported lower eNOS expression in preeclamptic syncytiotrophoblasts than in normal syncytiotrophoblasts [15,16], a series of clinical studies revealed that increased NO concentration primarily caused altered fetoplacental circulation, endothelial dysfunction, and reduced low-mediated vasodilatation in diferent pregnancy pathologies [17][18][19]. Moreover, these studies identiied increased endothelial permeability and decreased eNOS expression in the peripheral vasculature under pathological conditions [17].…”

Section: Speciication and Function Of Vascular Endothelium In Fetoplamentioning

confidence: 99%

Endothelial Nitric Oxide Synthase and Neurodevelopmental Disorders

Huseynova¹,

Panakhova²,

Hasanov³

et al. 2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Endothelial activity relects the balance of endogenous factors regulating vasoconstriction and vasodilation. Among these factors, nitric oxide (NO) is the most important contributor to the acute regulation of vascular tone. Altered nitric oxide synthesis by the vascular endothelium plays several important roles in the pathogenesis of neonatal disease through its efects on vascular homeostasis. However, the role of NO in the pathogenesis of perinatal brain injury has not been fully investigated. The present chapter explores how NO synthesis is regulated under physiological and pathological conditions, the impact of acute and chronic hypoxia on NO synthase activity in the vascular endothelium, and the role of perinatal endothelial dysfunction in the pathogenesis of neurodevelopmental disorders later in life.

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Reduced l-arginine Level and Decreased Placental eNOS Activity in Preeclampsia

Cited by 104 publications

References 28 publications

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Oxidative stress and inflammatory markers in normal pregnancy and preeclampsia

Endothelial Nitric Oxide Synthase and Neurodevelopmental Disorders

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