Potential role of endothelin-1 in normal and hypertensive pregnancies

Mastrogiannis, Dimitrios; O’Brien, William F.; Krammer, Judith; Benoit, Ray

doi:10.1016/0002-9378(91)90020-r

Cited by 84 publications

(44 citation statements)

References 25 publications

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“…One potential pathway by which glucocorticoids may promote vasoconstriction is via the potent vasoconstrictor peptide endothelin-1. Preeclampsia is associated with elevated endothelin-1 in both the maternal (36) and fetal compartments (37) and glucocorticoids have been shown to potentate its vasoconstrictive actions. The female fetus appears to be sensitive to changes in glucocorticoid exposure and therefore may exhibit increased placental vasoconstriction (38) and uteroplacental insufficiency.…”

Section: Resultsmentioning

confidence: 99%

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

2009

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This study aimed to characterize early neonatal microvascular function after preeclamptic pregnancy with respect to infant sex and in utero growth. Peripheral microvascular blood flow was examined prospectively from 6 to 72 h of age using laser Doppler flowmetry in a cohort of term infants of normotensive women and women with late-onset preeclampsia. For male infants, those born to preeclamptic women had greater microvascular blood flow at 6 h (p Ͻ 0.05) with no change over time. Male infants of normotensive women exhibited increasing blood flow with time (p ϭ 0.005). Female infants of preeclamptic mothers exhibited similar blood flow at 6 h of age to females of normotensive mothers, followed by significantly greater blood flow by 72 h (p Ͻ 0.001). Altered fetal microvascular structure and function in response to maternal preeclampsia may result in sexually dimorphic patterns of fetal growth and account for alterations in neonatal microvascular adaptation after birth.

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Section: Resultsmentioning

confidence: 99%

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

2009

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“…Indeed, plasma levels of ET-1 are elevated in preeclampsia as compared with normal pregnancy (Mastrogiannis et al, 1991;Nova et al, 1991;Clark et al, 1992). Furthermore, high levels of ET-1 are closely related with biological markers of renal impairment in preeclampsia (Clark et al, 1992).…”

Section: Resultsmentioning

confidence: 99%

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Sabry

Mondon

Lévy

et al. 1995

British J Pharmacology

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1 The aim of this study was to assess the role of endothelial cells in the modulation of vasocontractile responses to endothelin-1 (ET-1) of human placental vasculature.2 Isolated stem villi small arteries (diameter = 170-250 gm) were obtained from healthy parturients who underwent caesarean surgery during the 39th week of pregnancy for cephalo-pelvic disproportion. Isometric tension was measured in vascular rings mounted in a myograph system and challenged with ET-1 (10-12 to 10-6 M). 3 The vasocontractile response to ET-1 was significantly (P<0.0001) increased in endothelial-denuded (active tension= 1156 + 214 mN mm-') as compared with endothelial-preserved vascular rings (active tension = 458 ± 48 mN mm-1). This difference was significantly (P< 0.05) but only partly abolished by the NO synthase inhibitor N1'-nitro-L-arginine (L-NOARG, 10' M).4 In endothelial-preserved rings submaximally precontracted with 5-hydroxytryptamine (10-6 M), ET-1 (10-12 to 10-9 M) induced dose-dependent relaxation (maximum relaxation = 70 + 7%) at 10-9 M, which was followed, at higher doses (10-8 to 10-6 M), by a contraction. In contrast, no relaxation was seen in endothelial-denuded rings. The relaxation in rings with endothelium was significantly (P<0.001) reduced by L-NOARG (10-4 M). Moreover, it was totally abolished by combined pretreatment with L-NOARG (10-4 M) and the sulphonylurea glibenclamide (10' M). 5 In conclusion, endothelial cells modulate the vascular responses to ET-1 through the release of NO and a substance acting on the ATP-sensitive K+ channel of smooth muscle of stem villi small arteries from healthy parturients.

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“…The role of ET in pre-eclampsia is unclear, however, as contradictory reports exist concerning circulating ET levels in normotensive patients and those exhibiting this condition. Some reports have shown that prepro-ET-1 gene expression and plasma ET-1 levels are similar in both normal pregnancy and pre-eclampsia (Benigni et al, 1992;Otani et al, 1991), whilst others have reported elevated maternal plasma ET-1 levels in pre-eclampsia implicating ET in the impaired renal function and placental blood flow associated with the disease (Mastrogiannis et al, 1991;Nova et al, 1991;Clark et al, 1992). In the present study, we were unable to detect a difference in either the relative density or proportion of vascular and villous ET receptor imating the equilibrium dissociation constant from saturation data obtained under these conditions was therefore considered inappropriate.…”

Section: Discussionmentioning

confidence: 99%

“…Endothelin (ET) has been shown to be a potent vasoconstrictor of the human isolated foetoplacental cotyledon (Wilkes et al, 1990) and foetoplacental blood vessels (MacLean et al, 1992) and has the potential to influence placental blood flow either directly or in concert with other vasoactive agents including thromboxane A2, prostaglandin F2., prostacyclin, nitric oxide and atrial natriuretic peptide (De Nucci et al, 1988;Hu et al, 1988;Rae et al, 1989;Wilkes et al, 1990;Cameron et al, 1991). Circulating ET levels have been shown to increase during pregnancy and labour (Mastrogiannis et al, 1991); however, conflicting evidence exists concerning the possible role of ET in the pathogenesis of pre-eclampsia. While some reports have indicated a further elevation of plasma ET levels in this condition (Nova et al, 1991;Clark et al, 1992), more recent studies have not found a significant difference in plasma ET levels between pre-eclamptic and normal pregnancies (Benigni et al, 1992) nor any correlation between plasma ET-1 concentration, blood pressure or renal function during toxaemic pregnancy (Otani et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Differential localization of endothelin ET_a and ET_B binding sites in human placenta

Rutherford

Wharton

McCarthy

et al. 1993

British J Pharmacology

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1 The localization and differential distribution of endothelin (ET) receptor subtypes (ETA and ETB) was investigated in sections of human placenta by use of quantitative in vitro autoradiography and receptor selective ligands.2 Specific, high density ['251]-ET-1 binding sites were localized to the decidua and foetal membranes as well as to arteries and veins in the chorionic plate and throughout the villous tree. Moderate to low density binding was found in the extravillous and villous trophoblast respectively. 6 ET may have a local autocrine or paracrine role in the placenta, acting via specific receptors to influence foetoplacental blood flow and other aspects of placental function.

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Potential role of endothelin-1 in normal and hypertensive pregnancies

Cited by 84 publications

References 25 publications

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Differential localization of endothelin ET_a and ET_B binding sites in human placenta

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Potential role of endothelin-1 in normal and hypertensive pregnancies

Cited by 84 publications

References 25 publications

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

Neonates Born to Mothers With Preeclampsia Exhibit Sex-Specific Alterations in Microvascular Function

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Differential localization of endothelin ETa and ETB binding sites in human placenta

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Differential localization of endothelin ET_a and ET_B binding sites in human placenta