Reduced antioxidant capacity in second‐trimester pregnancies with pathological uterine perfusion

Stepan, Holger; Heihoff-Klose, A; Faber, R.

doi:10.1002/uog.1045

Cited by 18 publications

(15 citation statements)

References 18 publications

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“…Notably, an abnormal uterine perfusion characterizes pregnancies at risk for these pregnancy complications and precedes their clinical manifestation. However, only approximately one third of the pregnant women with abnormal uterine perfusion develop a complication, whereas the others have a normal course of pregnancy despite the high uteroplacental resistance (11).…”

Section: First Published Online March 28 2006mentioning

confidence: 99%

“…Independently other pregnant women with manifest pathology such as preeclampsia (18 patients) or isolated IUGR (nine patients) were recruited in the third trimester. The second-trimester Doppler investigations were performed using a LOGIQ 9 ultrasound machine (GE, Solingen, Germany) as described before (11). Preeclampsia was defined according to the guidelines of the International Society for the Study of Hypertension in Pregnancy (13).…”

Section: Experimental Subjectsmentioning

confidence: 99%

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Relation between Circulating Angiotensin II Type 1 Receptor Agonistic Autoantibodies and Soluble fms-Like Tyrosine Kinase 1 in the Pathogenesis of Preeclampsia

Stepan¹,

Faber²,

Wessel³

et al. 2006

The Journal of Clinical Endocrinology & Metabolism

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Section: First Published Online March 28 2006mentioning

confidence: 99%

Section: Experimental Subjectsmentioning

confidence: 99%

Relation between Circulating Angiotensin II Type 1 Receptor Agonistic Autoantibodies and Soluble fms-Like Tyrosine Kinase 1 in the Pathogenesis of Preeclampsia

Stepan¹,

Faber²,

Wessel³

et al. 2006

The Journal of Clinical Endocrinology & Metabolism

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“…Oxidative stress by this criterion is present in women with abnormal Doppler velocimetry whether they subsequently have preeclampsia, FGR or normal pregnancy outcomes. [37]…”

Section: Pathophysiological Markers Of Placental Dysfunctionmentioning

confidence: 99%

The placenta in preeclampsia

Roberts

Escudero

2012

Pregnancy Hypertension: An International Journal of Women's Car

367

249

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The root cause of preeclampsia is the placenta. Preeclampsia begins to abate with the delivery of the placenta and can occur in the absence of a fetus but with the presence of trophoblast tissue with hydatidiform moles. In view of this, study of the placenta should provide insight into the pathophysiology of preeclampsia. In this presentation we examine placental pathological and pathophysiological changes with preeclampsia and fetal growth restriction (FGR). It would seem that this comparison should be illuminating as both conditions are associated with similarly abnormal placentation yet only in preeclampsia is there a maternal pathophysiological syndrome. Similar insights about early and late onset preeclampsia should also be provided by such information. We report that the placental abnormalities in preeclampsia are what would be predicted in a setting of reduced perfusion and oxidative stress. However, the differences from FGR are inconsistent. The most striking differences between the two conditions are found in areas that have been the least studied. There are differences between the placental findings in early and late onset preeclampsia but whether these are qualitative, indicating different diseases, or simply quantitative differences within the same disease is difficult to determine. We attempt to decipher the true differences, seek an explanation for the disparate results and provide recommendations that we hope may help resolve these issues in future studies.

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“…Emerging evidence indicates that vascular functional and structural damage caused by yet to be identified mediators present in the maternal circulation of preeclampsia patients plays a causative role in the development of hypertension and proteinuria, two of the major symptoms in these patients [2]. In 1999, Wallukat et al [3] first reported that the autoimmune antibody against the second extracellular loop (165-191) of angiotensin II receptor type 1 (AT1-AA) is present in preeclamptic patients but not in healthy pregnancies or those with essential hypertension, and proposed that AT1-AA induces, similar to angiotensin II, an increase of the beating rate in spontaneously beating neonatal rat cardiomyocytes.…”

Section: Introductionmentioning

confidence: 99%

Autoantibody against AT1 receptor from preeclamptic patients induces vasoconstriction through angiotensin receptor activation

Yang¹,

Wang

Hai-liang

et al. 2008

Journal of Hypertension

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Preeclampsia is a serious pathologic complication during pregnancy, and its pathogenesis remains poorly understood. Recent studies have demonstrated that autoantibodies against angiotensin II type 1A receptor (AT1-AA) are present in women with preeclampsia. However, their role in the development of hypertension in preeclamptic patients has never been previously investigated. The present study was designed to determine whether AT1-AA isolated from the sera of preeclamptic patients causes vascular constriction and, if so, to further investigate the cellular receptors that mediate their vasoactivity. Blood samples were collected from 49 pregnant women (preeclampsia = 31, control = 18) and AT1-AA was detected using enzyme-linked immunosorbent assay. Vasoconstrictive effect of purified IgG from the sera of either preeclamptic patients or normal pregnant women was determined in isolated rat thoracic aorta, arteriae cerebri media and coronary artery. Compared with normal pregnant women, frequency of AT1-AA positive samples was markedly increased in preeclamptic patients (80.7 vs. 5.6%, P < 0.01). In isolated thoracic aortic rings, middle cerebral artery and coronary artery segments, AT1-AA induced vasoconstriction in a concentration-dependent fashion (P < 0.01). The vasoconstrictive effect of AT1-AA was completely blocked by losartan, an AT1-receptor antagonist. These data demonstrate that the AT1-AA causes significant vascular constriction in large conduit vessel as well as small resistant vessels though activation of the AT1 receptor. These results suggest that overproduction of AT1-AA is a novel risk factor in pregnant women and may play a causative role in the development of hypertension and vascular injury in preeclamptic patients.

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Reduced antioxidant capacity in second‐trimester pregnancies with pathological uterine perfusion

Abstract: Objectives

Cited by 18 publications

References 18 publications

Relation between Circulating Angiotensin II Type 1 Receptor Agonistic Autoantibodies and Soluble fms-Like Tyrosine Kinase 1 in the Pathogenesis of Preeclampsia

Relation between Circulating Angiotensin II Type 1 Receptor Agonistic Autoantibodies and Soluble fms-Like Tyrosine Kinase 1 in the Pathogenesis of Preeclampsia

The placenta in preeclampsia

Autoantibody against AT1 receptor from preeclamptic patients induces vasoconstriction through angiotensin receptor activation

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