Deficiency of c-Gmrp Level in Placental Circulation in Pregnancy-Induced Hypertensive Disorders: Possibility of Decreased Endothelium-Derived Relaxing Factor Activity

Kovacs, GÁBor Antal; Makdry, Anna; Pető, Judit; Steinmetz, Gyorgy

doi:10.3109/10641959409009569

Cited by 12 publications

(6 citation statements)

References 21 publications

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“…Also, sera from affected women are a more potent stimulant of NO production in normal endothelial cell culture than are sera from normotensive women (Baker et al 1995), indicating some form of a blockage of the NO-production pathway in the endothelium of these women, with activation of a feedback mechanism and accumulation of substances that stimulate NO synthesis. Recent studies show that cAMP production in the placental circulation is reduced in hypertensive pregnancies compared with pregnancies in normotensive women (Kovacs et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Evidence for a Familial Pregnancy-Induced Hypertension Locus in the eNOS-Gene Region

Arngrı́msson¹,

Hayward²,

Nadaud³

et al. 1997

The American Journal of Human Genetics

127

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Pregnancy-induced hypertension may be regarded as a manifestation of endothelial-cell dysfunction. The role of the eNOS gene in the development of a familial pregnancy-induced hypertension was evaluated by analysis of linkage among affected sisters and in multiplex families (n = 50). Markers from a 4-cM region encoding the eNOS gene showed distortion from the expected allele sharing among affected sisters (P = .001-.05), and the statistic obtained from the multilocus application of the affected-pedigree-member method also showed distortion (T[f(P)=sqrt(P)] = 3.53; P < .001). A LOD score of 3.36 was obtained for D7S505 when a best-fitting model derived from genetic epidemiological data was used, and LOD scores of 2.54-4.03 were obtained when various other genetic models were used. Estimates of recombination rate, rather than maximum LOD-score values, were affected by changes in the genetic parameters. The transmission-disequilibrium test, a model-free estimate of linkage, showed strongest association and linkage with a microsatellite within intron 13 of the eNOS gene (P = .005). These results support the localization of a familial pregnancy-induced hypertension-susceptibility locus in the region of chromosome 7q36 encoding the eNOS gene.

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Section: Discussionmentioning

confidence: 99%

Evidence for a Familial Pregnancy-Induced Hypertension Locus in the eNOS-Gene Region

Arngrı́msson¹,

Hayward²,

Nadaud³

et al. 1997

The American Journal of Human Genetics

127

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“…According to these authors, low L‐arginine levels may be of pathophysiological importance in these fetuses, resulting in decreased umbilical NO release. Kovacs et al 129 have shown reduced cGMP levels in the placental circulation in pregnancy‐induced hypertensive disorders.…”

Section: Pre‐eclampsiamentioning

confidence: 99%

Nitric oxide, the endothelium, pregnancy and pre‐eclampsia

Morris

Eaton

Dekker

1996

BJOG

148

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“…Histamine, a stimulator of nitric oxide release, relaxes umbilical arteries in vitro in early (from the 18th to the 32nd week) but not late gestation (from the 38th to the 41st week), suggesting decreased generation or response to nitric oxide during pregnancy 15 . Some investigators have proposed that nitric oxide synthase in the placenta and the release of endothelial derived vasodilators (EDRF) from umbilical vessels are reduced in pre‐eclampsia 16–18 . Others, however, have shown increased plasma and urine nitric oxide metabolites in women with pre‐eclampsia which positively correlated with changes in systolic blood pressure between the first and third trimesters 17,19 .…”

Section: Introductionmentioning

confidence: 99%

Systemic and fetal–maternal nitric oxide synthesis in normal pregnancy and pre‐eclampsia

Boccardo

Soregaroli

Aiello

et al. 1996

BJOG

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Objective To investigate systemic and fetal‐placental nitric oxide synthesis by biochemical and molecular biology means in normal human pregnancy and pre‐eclampsia. Design and participants Three groups of women were studied healthy pregnant women (n= 8), pregnant women with pre‐eclampsia (n= 8), and age‐matched nonpregnant controls (n= 8). Pre‐eclamptic patients were treated with nifedipine (30–60 mg/day) for severe hypertension. Systemic nitric oxide synthesis was assessed in normal pregnant women at weeks 18–21, 29–32 and 38–39 and in pre‐eclamptic women on admission to the hospital (29–32 weeks, 30 on average), before the morning nifedipine administration. Nonpregnant women were studied twice at four‐week intervals as controls. The pattern of nitric oxide biosynthesis in fetal‐placental circulation was studied in normal and pre‐eclamptic women at the delivery. Setting Mario Negri Institute for Pharmacological Research, Bergamo, and the Division of Obstetrics and Gynaecology of the University of Brescia. Main outcome measures Plasma cGMP levels and platelet nitric oxide synthesis, assessed by measuring the conversion of [3H]L‐arginine to [3H]L‐citrulline as well as intracellular cGMP, were evaluated. Constitutive nitric oxide synthase (EC‐NOS) gene expression by Northern blot analysis and nitric oxide release by the conversion of [3H]L‐arginine to [3H]L‐citrulline were assessed in umbilical vein endothelial cells (HUVEC) and in placenta. Inducible nitric oxide synthase activity was also evaluated in HUVEC exposed to tumour necrosis factor α (TNFα) and in placenta homogenates incubated in calcium free medium. Results Plasma cGMP was higher in both normal pregnant and pre‐eclamptic women than in nonpregnant controls. In normal pregnancy cGMP rose as early as 18–21 weeks and remained elevated throughout pregnancy. [3H]L‐citrulline production and intracellular cGMP were comparable in platelets from all women. EC‐NOS gene expression and nitric oxide synthesis were identical in HUVEC and placenta from normal pregnant and pre‐eclamptic women. Conclusions Systemic levels of cGMP, the nitric oxide second messenger, are increased in normal pregnancy. Excessive nitric oxide production does not derive from platelets. Pre‐eclampsia is not associated with changes in fetal‐placental nitric oxide synthesis.

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Deficiency of c-Gmrp Level in Placental Circulation in Pregnancy-Induced Hypertensive Disorders: Possibility of Decreased Endothelium-Derived Relaxing Factor Activity

Cited by 12 publications

References 21 publications

Evidence for a Familial Pregnancy-Induced Hypertension Locus in the eNOS-Gene Region

Evidence for a Familial Pregnancy-Induced Hypertension Locus in the eNOS-Gene Region

Nitric oxide, the endothelium, pregnancy and pre‐eclampsia

Systemic and fetal–maternal nitric oxide synthesis in normal pregnancy and pre‐eclampsia

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