Plasma Asymmetric Dimethylarginine Concentration during the Perinatal Period

Vida, Gabriella; Sulyok, E.; Ertl, Tibor; Martens‐Lobenhoffer, Jens; Bode‐Böger, Stefanie M.

doi:10.1159/000098411

Cited by 25 publications

(20 citation statements)

References 42 publications

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“…For ADMA and L-arginine concentrations, there were consistent veno-arterial differences, with higher levels in the umbilical vein compared with the umbilical artery, suggesting that these metabolites are mainly placentally derived, not fetally, which is consistent with a study performed in normal infants (37). ADMA and SDMA may be derived from the placenta, but may also be concentrated from the maternal plasma; it is not possible to discern between these possibilities from this study.…”

Section: Discussionsupporting

confidence: 83%

“…ADMA and SDMA may be derived from the placenta, but may also be concentrated from the maternal plasma; it is not possible to discern between these possibilities from this study. The very high concentration of ADMA in the fetal circulation is an enigma, and it has been hypothesized that it is a compensatory mechanism to stabilize very high NO concentrations in the fetoplacental unit (30,37).…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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“…Mittermayer et al [8] reported that male preterm newborns had significantly higher umbilical venous blood concentrations of ADMA than did female preterm newborns and term newborns of both sexes. Vida et al [9] reported that ADMA concentrations in umbilical blood from term newborns were elevated with a consistent venoarterial difference, suggesting that the high levels of ADMA in umbilical blood are mainly generated by the placenta. These 3 groups of investigators used HPLC for analyses.…”

Section: Discussionmentioning

confidence: 99%

“…Determination of ADMA concentrations in umbilical blood might be important to elucidate the regulatory mechanisms of the circulatory system in this particular period. Only 3 studies have measured umbilical blood concentrations of ADMA [7][8][9]. Asymmetric dimethylarginine in umbilical blood appears significantly higher than the maternal levels when delivery occurs at term or preterm.…”

Section: Introductionmentioning

confidence: 99%

Determination of asymmetric dimethylarginine, an endogenous nitric oxide synthase inhibitor, in umbilical blood

Tsukahara¹,

Ohta²,

Tokuriki³

et al. 2008

Metabolism

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“…In gestational diabetes, the risk continues after birth, and those women are considered to have a high risk of cardiovascular disease [28]. There is a previous study on the importance of ADMA in fetoplacental and neonatal circulation [29]. In this study, placental macro and microvascular endothelial dysfunction was established in diabetic pregnant women, but no clear information could be obtained on this subject [20,21].…”

Section: Discussionmentioning

confidence: 84%

Impairment of Glucose Tolerance Test During Pregnancy and Serum Assymmetric Dimethylarginine Levels

Fındık¹

2016

Ann Clin Anal Med

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ÖzetAmaç: Asimetrik dimetilarjinin (ADMA), nitrik oksit sentaz (NOS) inhibitörü olup endotel disfonksiyonunu göstermektedir. ADMA diabetli hastalarda yük-sek tespit edilmiştir. Bu çalışmada amacımız, normal glukoz toleranslı, bozulmuş glukoz toleranslı ve gestasyonel diabetli gebe hastalardaki serum ADMA ve Arjinin düzeyleri arasındaki farkları tespit etmek ve serum ADMA ve Arjininin bebek kiloları ile ilişkisini araştırmaktır. Gereç ve Yöntem: Çalışmamı-za 50 gr glukoz tolerans testi normal olan 64 gebe (grup 1 ,NGT); 50 gr testi yüksek ve 100 gr oral glukoz testi (OGTT) normal olan 33 gebe ( bu grup bozulmuş glukoz toleransı olan grup olarak da adlandırılmaktadır) ( grup 2, IGT) ; ve gestasyonel diabetli 8 gebe (GDM, grup 3) dahil edildi. Gebelerin serum ADMA ve Arjinin düzeyleri araştırıldı. Bu üç grup arasında istatiksel analiz yapıldı. Bulgular: Serum Arjinin düzeyleri bozulmuş glukoz toleransı olan grupta (IGT), NGT grubundan anlamlı derecede yüksekti. ADMA düzeyleri GDM grubunda yüksekti ancak istatistiksel olarak anlamlı kabul edilmedi. Arginin ve ADMA düzeyleri arasında korelasyon tespit edildi (r = 0.219; p<0.05). Ayrıca serum ADMA düzeyleri ile ailesel diabet öyküsü arasında istatistiksel olarak anlamlı ilişki tespit edildi (r = 0.217; p<0.05). ADMA, Arjinin düzeyleri ve bebek kiloları arasında ilişki bulunamadı. Tartışma: Bozulmuş glukoz toleranslı (IGT) ve gestasyonel diabeti (GDM) olan grupta ADMA yükselme eğilimin-dedir. Bu yükseliş klinik olarak önemli olmasa da, nitrik oksit eksikliğini gös-teren bir durum olup, özellikle ailesel diabet öyküsü olan, beden kitle indeksi artmış ve ileri yaş gebeliklerde daha belirgindir. Buna bağlı olarak da bu gebelerde daha dikkatli monitorizasyon ve takip gereklidir. Artan ADMA ve Arjinin düzeyleri bebek kilosunu etkilemiyor görünmektedir.. Anahtar KelimelerAsimetric Dimetilarjinin; Gestasyonel Diabet; Bozulmuş Glukoz Toleransı; Endotel Disfonksiyon; Arjinin Abstract Aim: Assymetric dimethylarginin (ADMA), an inhibitor of nitric oxide synthase (NOS), has been linked to endothelial dysfunction. Our aim in this study was to compare ADMA and arginine levels in normal glucose tolerance, impaired glucose tolerance and gestational diabetes groups and investigate the effect on baby birth weight. Material and Method: Serum ADMA and arginine levels were investigated in 64 patients whose 50-g glucose loading test was normal (group 1, NGT); 33 patients whose 50-g test result was high and those whose 100-g oral glucose tolerance test (OGTT) was normal, namely, those with impaired glucose tolerance (IGT, group 2) ; and in 8 patients diagnosed with gestational diabetes mellitus (GDM, group 3). Results: Arginine levels were significantly higher in the IGT group than in the NGT group. ADMA levels were high in the GDM group, but the difference was not statistically significant. There were a statistically significant correlation between arginine and ADMA levels and the ADMA level of those with a diabetes history. No significant relationship was found between ADMA level, arginine...

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Plasma Asymmetric Dimethylarginine Concentration during the Perinatal Period

Cited by 25 publications

References 42 publications

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Determination of asymmetric dimethylarginine, an endogenous nitric oxide synthase inhibitor, in umbilical blood

Impairment of Glucose Tolerance Test During Pregnancy and Serum Assymmetric Dimethylarginine Levels

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