Nitric Oxide Metabolites in Normal Human Pregnancy and Preeclampsia

Curtis, Narelle E; Gude, Neil M; King, Roger G; Marriott, Philip J.; Rook, Trevor J.; Brennecke, Shaun

doi:10.3109/10641959509015680

Cited by 51 publications

(16 citation statements)

References 40 publications

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“…6,7 Recent clinical studies in humans, however, have conflicting results with regard to the role of nitric oxide in preeclampsia. [8][9][10][11] Since vascular tone is largely determined by the activity of the sympathetic nervous system, we decided to examine whether an increase in sympathetic vasoconstrictor activity may be an important mechanism in mediating the increase in peripheral vascular resistance in preeclampsia. We therefore measured postganglionic action potentials in sympathetic-nerve fibers innervating blood vessels in the skeletal muscle in patients with preeclampsia.…”

Section: Resultsmentioning

confidence: 99%

Preeclampsia — A State of Sympathetic Overactivity

et al. 1996

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Section: Resultsmentioning

confidence: 99%

Preeclampsia — A State of Sympathetic Overactivity

et al. 1996

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“…Evidence supporting this hypothesis includes the finding that the administration of NOS inhibitors to pregnant rats induces hypertension and proteinuria, which are reminiscent of pre-eclampsia [4,5] . However, other investigators have reported that NO production is enhanced or unchanged in severe pre-eclampsia [6][7][8] .…”

Section: Introductionmentioning

confidence: 91%

Analysis of Nitric Oxide Metabolism as a Placental or Maternal Factor Underlying the Etiology of Pre-Eclampsia

Nishizawa¹,

Pryor-Koishi²,

Suzuki³

et al. 2009

Gynecol Obstet Invest

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Background:Defective nitric oxide (NO)-mediated vasodilation is widely regarded as an underlying cause of hypertension in pre-eclampsia, although there are also arguments against this hypothesis. Methods:We examined both the mRNA levels and the presence of a Glu298Asp substitution in the NO synthase (NOS) gene, as well as the NO metabolite concentration, in placentas and maternal sera from women with pre-eclampsia and in normotensive pregnant controls (25–40 vs. 24–41 weeks of gestation). Results:Pre-eclamptic and control placentas did not show any significant differences in their NO metabolite levels or their NOS expression levels as measured by quantitative RT-PCR. In addition, we did not find any association between pre-eclampsia and the occurrence of the Glu298Asp amino acid substitution in the NOS gene. In contrast, high maternal circulating NO metabolites were evident in severe pre-eclampsia (p < 0.0001). Although a positive correlation between circulating NO metabolites and blood pressure was not observed, uterine artery resistance measured by ultrasound was found to positively correlate with the maternal NO levels. Conclusions:Our current data suggest that an altered placental NOS pathway is unlikely to be the primary cause of pre-eclampsia and that the activation of this pathway is possibly in response to maternal symptoms.

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“…NO may also play a role in maintaining low fetal vascular resistance, as well as attenuating the actions of vasoconstrictors, in the human placenta [9-111. Although it has been postulated that reduced production of NO is an important feature of preeclampsia and contributes to the disturbance in levels and reactivity of vasoactive substances, supportive evidence is inconclusive [3]. Plasma measurement of the nitrite and nitrate metabolites of NO have shown both reduction [12] and no change [13] in pre-eclampsia compared with normal pregnancy. In addition, urinary nitrite and nitrate levels, as well as cyclic GMP levels, were found not to change with pre-eclampsia [14-161.…”

Section: Introductionmentioning

confidence: 99%

Reduction of Placental Nitric Oxide Synthase Activity in Pre-Eclampsia

et al. 1997

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1. The role of the potent vasodilator nitric oxide in the pathogenesis of pre-eclampsia is unclear. We have tested the hypothesis that placental activity of the enzyme which synthesizes nitric oxide (nitric oxide synthase) is reduced in pre-eclampsia. 2. Placentae were obtained after vaginal delivery or Caesarean section from women who had been assigned to the following groups according to standard obstetric criteria: term non-pre-eclamptic control, term pre-eclamptic, preterm non-pre-eclamptic control and preterm pre-eclamptic. Nitric oxide synthase activity of placental tissue homogenates was assessed by measuring conversion of [3H]L-arginine into [3H]L-citrulline in the presence of NADPH, FAD, tetrahydrobiopterin, calmodulin, CaCl2, magnesium acetate and a range of L-arginine concentrations. Michaelis Menton constants (K(m)) amd maximum velocities of reaction (Vmax) were calculated using Lineweaver-Burk analysis. 3. Vmax was significantly reduced in both term and preterm pre-eclamptic placentae compared with placentae from corresponding gestation-matched controls. There were no significant differences in the K(m) values for nitric oxide synthase between any of the four groups, nor were Vmax or K(m) values significantly influenced by mode of delivery. 4. These results provide evidence that human placental nitric oxide synthase activity is significantly reduced in pre-eclampsia. Such a reduction was evident at both term and preterm gestations. Reduced placental nitric oxide synthase activity may have an adverse effect on placental haemodynamic function in pre-eclampsia, and could be involved in the pathogenesis of this important and common obstetric complication.

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Nitric Oxide Metabolites in Normal Human Pregnancy and Preeclampsia

Cited by 51 publications

References 40 publications

Preeclampsia — A State of Sympathetic Overactivity

Preeclampsia — A State of Sympathetic Overactivity

Analysis of Nitric Oxide Metabolism as a Placental or Maternal Factor Underlying the Etiology of Pre-Eclampsia

Reduction of Placental Nitric Oxide Synthase Activity in Pre-Eclampsia

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