Differential Nitric Oxide Synthase Activity in Human Platelets during Normal Pregnancy and Pre-Eclampsia

Delacrétaz, Etienne; Quay, N de; Waeber, Bernard; Vial, Yvan; Schulz, Pierre-E.; Burnier, Michel; Brunner, Hans R.; Bossart, H.; Schaad, Nicolas

doi:10.1042/cs0880607

Cited by 40 publications

(26 citation statements)

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“…This is further supported by previous findings of reduced levels of ADMA and enhanced endothelial function, as assessed by flow-mediated dilatation and venous occlusion plethysmography, in normal pregnancy. 26 -28 Such NO-mediated vasodilation, possibly induced by estrogen, 21,22,29 may increase reflection site distance within the vasculature and reduce wave reflection amplitude; thus explaining the reduction in AIx. This contention is supported by the increase in pulse wave transient time observed in our pregnant population.…”

Section: Macedo Et Al Arterial Stiffness In Normal Pregnancymentioning

confidence: 99%

“…21,22 Indeed, inhibition of NO by intravenous infusion of L-N Gmonomethyl arginine results in increased AIx. 23 Augmentation index has recently been shown to be positively associated with asymmetrical dimethyl-arginine (ADMA), an endogenous inhibitor of NO synthase 24 and inversely correlated with global endothelial function, 25 which is NO dependent.…”

Section: Macedo Et Al Arterial Stiffness In Normal Pregnancymentioning

confidence: 99%

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Maternal Wave Reflections and Arterial Stiffness in Normal Pregnancy as Assessed by Applanation Tonometry

et al. 2008

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Abstract-Normal pregnancy is associated with profound alterations in the maternal cardiovascular system. The aim of the present study was to assess noninvasively, using applanation tonometry, the maternal central aortic blood pressures (BP), effects of wave reflection and arterial stiffness (aortic and brachial pulse wave velocity) in normal pregnancy. This was a cross sectional study including 193 women with normal singleton pregnancies at 11 to 41 weeks of gestation and 23 nonpregnant controls, matched for age and height. Pϭ0.007). This change was present even after adjusting for maternal age (PϽ0.001), heart rate (PϽ0.001), and mean arterial BP (PϽ0.001); known determinants of AIx. The pulse wave velocity (carotid-radial and carotid-femoral) did not change significantly with gestation and was marginally different between pregnant and nonpregnant women (Pϭ0.03 and Pϭ0.05 for carotid-radial and carotid-femoral respectively). However, adjustments for maternal age and mean arterial pressure rendered these differences nonsignificant (Pϭ0.2 for carotid-radial, Pϭ0.5 for carotid-femoral). In summary, we found that normal pregnancy is associated with a reduction in central BP and wave reflection. Key Words: pregnancy Ⅲ applanation tonometry Ⅲ arterial stiffness Ⅲ augmentation index Ⅲ pulse wave velocity N ormal pregnancy is associated with increased intravascular volume, cardiac output, and heart rate, a marked decrease in vascular resistance and a tendency toward decreased mean blood pressure (BP). [1][2][3][4] The decrease in peripheral vascular resistance and generalized vasodilation is associated with increased aortic distensibility. 5,6 However, there is scanty information regarding maternal central hemodynamics and arterial stiffness. Noninvasive assessment of arterial stiffness is possible by the simple, validated, and reproducible technique of applanation tonometry. 7,8 Using this technique pulse wave analysis (PWA) and pulse wave velocity (PWV) can be carried out. With PWA of the radial artery waveform, it is possible to assess central pressures and augmentation index (AIx), a measure of arterial wave reflection whereas with PWV it is possible to measure the stiffness in the carotid-radial (muscular) and carotid-femoral (elastic) part of the arterial tree. Several studies in nonpregnant populations have shown that arterial stiffness is increased in patients with risk factors for cardiovascular disease such as hypertension, hypercholesterolemia, and diabetes mellitus. 9 -11 Additionally, 3 studies in pregnancy suggested that preeclampsia is characterized by increased maternal arterial stiffness. 12,13,14 The aim of the present study was to assess the influence of normal pregnancy on maternal central pressures, arterial wave reflection, and stiffness using applanation tonometry. Methods SubjectsThis was a cross sectional study involving 193 pregnant women with singleton pregnancies at 11 to 41 weeks of gestation and 23 healthy nonpregnant controls. The subjects were recruited from the routine antenatal clinic...

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Section: Macedo Et Al Arterial Stiffness In Normal Pregnancymentioning

confidence: 99%

Section: Macedo Et Al Arterial Stiffness In Normal Pregnancymentioning

confidence: 99%

Maternal Wave Reflections and Arterial Stiffness in Normal Pregnancy as Assessed by Applanation Tonometry

et al. 2008

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“…There is also evidence that endothelial cell dysfunction is present in women with a pre-eclamptic syndrome and that the resulting decrease in NO but also in prostacyclin synthesis is responsible for the clinical disorders characterizing preeclampsia, i.e., a reduced placental perfusion, an increased sensitivity to vasopressor agents, an activation of the coagulation cascade (Roberts et al, 1991;Rutherford et al, 1995;Baker et al, 1996) and a progressive increase in peripheral resistance and in blood pressure. Thus, a reduced NO synthesis linked to a decreased NO synthase expression or activity has been reported in pre-eclamptic patients (Pinto et al, 1991;Seligman et al, 1994;Delacretaz et al, 1995) although it is disputed by others (Baker et al, 1995). Moreover, the plasma of pre-eclamptic patients has been shown (a) to contain a fraction that inhibits the ability of acetylcholine to relax precontracted rabbit aortic rings (Pinto et al, 1992), but also (b) to reduce endothelial prostacyclin production (Ramsay et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Lack of beneficial effects of the NO‐donor, molsidomine, in the L‐NAME‐induced pre‐eclamptic syndrome in pregnant rats

Richer¹,

Boulanger²,

Es-Slami³

et al. 1996

British J Pharmacology

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1 In pregnant rats, chronic NO-synthase inhibition induces the development of a pre-eclamptic syndrome, characterized by an increase in maternal blood pressure, a loss of vascular refractoriness to pressor stimuli, a reduction in litter size and a decrease in pups (and maternal) weight. We investigated whether a NO-donor, molsidomine, administered during NO synthase inhibition, could restore a normal pregnancy.2 Pregnant rats were given daily, starting from day 14 of gestation, saline (controls), or L-NAME (50 mg kg-' d-'), or molsidomine (15 or 30 mg kg-' d-'), or the L-NAME + molsidomine combinations. Maternal blood pressure and body weight, litter size, pups weight and vascular reactivity to pressor stimuli (angiotensin II, noradrenaline, electrical stimulation of the spinal cord) were investigated. 3 L-NAME alone, as compared to controls, increased maternal blood pressure, reduced litter size (-59%), increased foetal reabsorptions (+ 625%) and decreased foetal weight (-10%). Vascular reactivity to pressor stimuli was enhanced. 4 Molsidomine alone, as compared to controls, dose-dependently decreased maternal blood pressure but had no effect on vascular reactivity and, whatever the dose, on foetal outcome. 5 The L-NAME-molsidomine combinations dose (of molsidomine)-dependently limited the rise in maternal blood pressure induced by L-NAME alone but unexpectedly, dose-dependently and significantly worsened pregnancy evolution, e.g., at 30 mg kg-'d-': litter size (-80%), foetal reabsorptions (+ 1025%), foetal weight (-24%). Vascular reactivity to pressor stimuli was paradoxically further enhanced. 6 Thus, in a chronic NO deprivation-induced model of pre-eclampsia in rats, molsidomine, possibly because of its hypotensive action, worsens the foetal outcome, which questions the usefulness of NOdonors in pre-eclamptic women.

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“…Several investigators have reported various risk factors to the causes of this prenatal group of conditions including preeclampsia, PIH, ecclampsia, abruption placentae, and HELLP syndrome, [3][4][5][6][7][8][9][10][11][12]. Coagulopathy is one of the major risk factors, and several authors have reported genetic polymorphisms including vascular endothelial growth factor, prothrombin gene polymorphisms, methylenetetrahydrofolate reductase, factor V Leiden, several interleukins, and polymorphisms in the genes involved in nitric oxide synthesis, [3][4][5][6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

“…Coagulopathy is one of the major risk factors, and several authors have reported genetic polymorphisms including vascular endothelial growth factor, prothrombin gene polymorphisms, methylenetetrahydrofolate reductase, factor V Leiden, several interleukins, and polymorphisms in the genes involved in nitric oxide synthesis, [3][4][5][6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Infant ENOS haplotypes and maternal PIH

Yanamandra¹,

Pramanik²,

Ja³

et al. 2017

Birth Defect

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To determine whether the fetal genotypes influence maternal circulation during pregnancy and induce preeclampsia. Although the etiology of Pregnancy induced hypertension (PIH) is unclear, endothelial dysfunction leading to hypercoagulability is a major contributing factor. Endothelial nitric oxide (eNO) serves as a vasodilator, relaxing smooth muscle, preventing platelet aggregation, and thus facilitating improved blood flow. Mutant eNO synthetase (eNOS) genotypes result in reduced nitric oxide levels. ENOS polymorphism in the mother has been considered to be a risk factor for preeclampsia. However, the off-springs have not been studied. The present study was undertaken to determine whether the fetal and / or maternal genotypes influence circulation during preeclampsia. ENOS SNPs assays were carried out on one hundred and seventy -five infants admitted to the Neonatal Intensive Care Unit at LSU Health Sciences Center. We found significant differences in eNOS gene frequencies between Caucasian and African American infants (p=<0.001 for combined SNPs). Our data also showed a marked increase (2 to 4 fold) in both SNP allele frequencies in Caucasian infants compared to controls (p=<0.01). The elevations in African American infants with maternal history of PIH were even more pronounced (p=<0.001).

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Differential Nitric Oxide Synthase Activity in Human Platelets during Normal Pregnancy and Pre-Eclampsia

Cited by 40 publications

References 0 publications

Maternal Wave Reflections and Arterial Stiffness in Normal Pregnancy as Assessed by Applanation Tonometry

Maternal Wave Reflections and Arterial Stiffness in Normal Pregnancy as Assessed by Applanation Tonometry

Lack of beneficial effects of the NO‐donor, molsidomine, in the L‐NAME‐induced pre‐eclamptic syndrome in pregnant rats

Infant ENOS haplotypes and maternal PIH

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