Plasma nitric oxide, endothelin‐1, arginase and superoxide dismutase in pre‐eclamptic women

Bernardi, Fabiana; Constantino, Larissa; Machado, Roberta; Petronilho, Fabrícia; Dal‐Pizzol, Felipe

doi:10.1111/j.1447-0756.2008.00860.x

Cited by 72 publications

(51 citation statements)

References 31 publications

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“…NO is a potent vasodilator that acts to induce relaxation in vascular smooth muscle cells via a cyclic guanosine monophosphate pathway (44). Decreased levels of NO (45,46) and increased levels of arginase (which degrades a precursor molecule in the NOS pathway) have been reported in preeclampsia (47,48). A deficiency in NO has been shown to correlate with metabolic derangements seen in preeclampsia, such as hypertension, proteinuria, and platelet dysfunction (45).…”

Section: Nitric Oxide Pathwaymentioning

confidence: 99%

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Phipps

Prasanna

Brima

et al. 2016

CJASN

489

328

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Preeclampsia is becoming an increasingly common diagnosis in the developed world and remains a high cause of maternal and fetal morbidity and mortality in the developing world. Delay in childbearing in the developed world feeds into the risk factors associated with preeclampsia, which include older maternal age, obesity, and/or vascular diseases. Inadequate prenatal care partially explains the persistent high prevalence in the developing world. In this review, we begin by presenting the most recent concepts in the pathogenesis of preeclampsia. Upstream triggers of the well described angiogenic pathways, such as the heme oxygenase and hydrogen sulfide pathways, as well as the roles of autoantibodies, misfolded proteins, nitric oxide, and oxidative stress will be described. We also detail updated definitions, classification schema, and treatment targets of hypertensive disorders of pregnancy put forth by obstetric and hypertensive societies throughout the world. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a selflimited occurrence. At the very least, we now know that preeclampsia does not end with delivery of the placenta. We conclude by summarizing the latest strategies for prevention and treatment of preeclampsia. A better understanding of this entity will help in the care of at-risk women before delivery and for decades after.

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Section: Nitric Oxide Pathwaymentioning

confidence: 99%

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Phipps

Prasanna

Brima

et al. 2016

CJASN

489

328

View full text Add to dashboard Cite

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“…In normal pregnancy, by 10 to 12 weeks of gestation, the onset of maternal blood flow in the placenta results in a local increase in oxygen tension and parallel elevation in the expression and activity of the antioxidant enzymes [13]. On the contrary, the increased concentration of superoxide in the placental tissue of preeclamptic women was found associated with decreased activity and plasma levels of SOD mRNA expression [14], [15]. Levels of gluthatione peroxidase were also found to be decreased in PE and could be associated with increased generation of toxic lipid peroxides contributing to the endothelial dysfunction and hypertension of PE [16], [17].…”

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confidence: 99%

Antioxidant Status in Normal Pregnancy and Preeclampsia upon Multivitamin-Mineral Supplementation in the Region of Vojvodina

Ćebović¹,

Marić²,

Nikolić³

et al. 2013

IJBBB

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Abstract-Normal pregnancy is associated with oxidative stress and this is even increased during preeclampsia (PE). The decrease in total antioxidant capacity is the pathophysiological basis for vitamin supplementation during pregnancy, but the beneficial effect of this approach is still unclear. Levels of creatinine, urea, cystatin, malondialdehyde (MDA), superoxide dysmutase activity (SOD), glutathione peroxidase (GSH-Px) activity and acidum ascorbicum were measured in the serums of all women. Mean MDA level in maternal plasma in normal pregnancies was significantly lower than in PE pregnancies (2,78 ±0.78 pmol/mg vs 3.20±0.91 pmol/mg, p< 0.05), as well as mean GSH-Px levels (811 ±206 U/l vs 1350±575 U/l, p< 0.05. Mean ascorbic acid values were significantly higher in normal than in PE pregnancies (9,85 ±2,43 mg/L vs 5.54±1.81 mg/L, p< 0.001), as well as mean SOD values (26.8 ±18.45% vs 12.3±10.3%, p< 0.001). There were no significant differences in normal pregnancy group with and without multivitamin supplementation. MDA levels were significantly lower in PE pregnancies with vitamin supplementation (2.99 ± 0.81 pmol/mg vs 3.42 ± 1.01 pmol/mg, p< 0.05), as well as GSC-Px levels (1200 ± 500 U/l vs 1500 ± 650 U/l, p< 0.05). Ascorbic acid values were significantly higher in the PE group with vitamin supplementation (6.16 ± 1.66 mg/L vs 4.92 ± 1.96 mg/L, p< 0.05), as well as SOD levels (13 ± 11.4 % vs 11.6 ± 9.2%, p< 0.001).

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“…3 Indeed, circulating levels of this highly potent vasoconstrictor have been shown to be significantly increased in women with preeclampsia compared with normal pregnant women. 4 Recently, ET-1 signaling has been shown to be involved in the pathophysiology of animal models of preeclampsia, such as the reduced uterine perfusion pressure (RUPP) model. 5,6 The production of ET-1 involves enzymatic cleavage of big ET-1 (bET-1), largely via ET converting enzymes (ECEs).…”

mentioning

confidence: 99%

Matrix Metalloproteinase Enhances Big-Endothelin-1 Constriction in Mesenteric Vessels of Pregnant Rats With Reduced Uterine Blood Flow

et al. 2013

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Abstract-Preeclampsia is a leading cause of maternal and fetal morbidity/mortality; however, the pathophysiological mechanisms are unclear. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs; particularly MMP-2), cleave the inactive precursor big ET-1 (bET-1) to active ET-1. Notably, expression levels of MMP-2 have been shown to be on the increase in women who subsequently develop preeclampsia. We hypothesized that the increased MMP-2 expression leads to increased bET-1 conversion, thereby increasing vasoconstriction in preeclampsia. A reduced uteroplacental perfusion pressure (RUPP) model of preeclampsia in the rat was used to assess mesenteric artery vascular function. Responses to bET-1 (3-310 nmol/L) and ET-1 (1-200 nmol/L) were studied in the presence or absence of inhibitors of enzymes known to cleave bET-1. Vascular contractility in response to bET-1 was greater in RUPP than Sham (P<0.001), whereas neither responses to ET-1 nor maximal contractility to high potassium salt solution (123.70 mmol/L) were different. MMP inhibition with GM6001 (30 μmol/L) significantly decreased responses to bET-1 in RUPP (P<0.001) but not Sham-operated rats. Interestingly, combined treatment with GM6001 and L-NG-nitroarginine methyl ester (100 μmol/L) revealed a NO modulation of MMPs that was reduced in RUPP. In summary, we found increased vascular contractility to bET-1 in the RUPP model of preeclampsia that was likely attributable to upstream enzymatic pathways. These data are consistent with a greater contribution of MMP to cleavage of bET-1 to ET-1 ex vivo in RUPP, suggesting that this enzyme may be partially responsible for increased bET-1-induced contractility.

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Plasma nitric oxide, endothelin‐1, arginase and superoxide dismutase in pre‐eclamptic women

Abstract: We suggested that in pre-eclampsia excessive arginase and low superoxide dismutase activity leads to a decrease nitric oxide levels and oxidative stress, and this may promote microvascular oxidative damage and endothelial dysfunction.

Cited by 72 publications

References 31 publications

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Antioxidant Status in Normal Pregnancy and Preeclampsia upon Multivitamin-Mineral Supplementation in the Region of Vojvodina

Matrix Metalloproteinase Enhances Big-Endothelin-1 Constriction in Mesenteric Vessels of Pregnant Rats With Reduced Uterine Blood Flow

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