Women with Preeclampsia Have Higher Plasma Endothelin Levels than Women with Normal Pregnancies

Taylor, Robert N.; Varma, Madhu; Teng, Nelson N.H.; Roberts, James M.

doi:10.1097/00006254-199107000-00005

Cited by 51 publications

(74 citation statements)

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“…Because endothelial damage is a known stimulus for ET-1 synthesis, increases in the production of ET-1 and activation of ET A receptors have been proposed to participate in the pathophysiology of hypertension during preeclampsia 28. A role for ET-1 in mediating the pathophysiology induced by placental ischemia has been demonstrated by previous studies performed in our laboratory.…”

Section: Discussionmentioning

confidence: 76%

Hypertension in Response to Chronic Reductions in Uterine Perfusion in Pregnant Rats

et al. 2008

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Abstract-Reductions in uterine perfusion pressure (RUPP) in pregnant rats is associated with increased tumor necrosis factor-␣ (TNF-␣). This study was designed to determine the role of endogenous TNF-␣ in mediating changes in arterial pressure and endothelin-1 (ET-1) in RUPP rats. To achieve this goal we examined the effect of RUPP in the presence and absence of a TNF-␣-soluble receptor, etanerecept (0.4 mg/kg). Mean arterial pressure increased from 102Ϯ1 mm Hg in normal pregnant (NP) rats to 134Ϯ3 mm Hg (PϽ0.05) in RUPP rats. Serum TNF-␣ increased to 40Ϯ7.6 pg/mL in RUPP rats (nϭ24)

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Section: Discussionmentioning

confidence: 76%

Hypertension in Response to Chronic Reductions in Uterine Perfusion in Pregnant Rats

et al. 2008

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“…Another vasoconstrictor that may be present in the pregnant plasma used in our experiments is ET-1. It has been postulated that increased levels of ET-1 may be capable of counteracting the vasodilatory effect on NO 20, 21. Perhaps the most likely candidate for a vasoconstrictor enabling pregnant plasma used in our study to elicit increased myogenic reactivity and tone in NP arteries is Ang II.…”

Section: Discussionmentioning

confidence: 91%

Resistance Artery Adaptation to Pregnancy Counteracts the Vasoconstricting Influence of Plasma From Normal Pregnant Women

et al. 2010

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Using a rat model, we investigated the effects of circulating factors in pregnancy on cerebrovascular and systemic vascular function by comparing myogenic reactivity, tone, and endothelial vasodilator production of the posterior cerebral artery (PCA) and mesenteric artery (MA) of nonpregnant animals perfused with nonpregnant and pregnant human plasma. Arteries from late pregnant (LP) animals were then perfused similarly to evaluate a potential adaptive effect of pregnancy on vessel function. A three-hour exposure to pregnant plasma caused increased myogenic reactivity and tone in vessels from NP animals and produced a decreased endothelium-derived hyperpolarizing factor response in nonpregnant PCAs, findings that were not seen with MAs. The increased reactivity and tone noted in nonpregnant vessels was abolished when pregnant plasma was perfused through LP arteries, suggesting these vessels adapt during pregnancy to the vasoconstricting influence of pregnant plasma.

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“…Also, ET-1 secretion is 4- to 8-fold higher in umbilical cord ECs of PE than Norm-Preg women [151]. The elevated plasma levels of ET-1 in PE women return to normal levels within 48 h of delivery, suggesting that ET-1 may contribute to the vasoconstriction and HTN in PE [152]. Typically, plasma levels of ET-1 are highest during the later stage of the disease, suggesting that ET-1 may not be involved in the initiation of PE, but rather in the progression of the disease into a malignant phase [93].…”

Section: Increased Endothelium-derived Vasoconstriction In Pementioning

confidence: 99%

Molecular and Vascular Targets in the Pathogenesis and Management of the Hypertension Associated with Preeclampsia

Reslan¹,

Khalil²

2010

CHAMC

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Normal pregnancy is associated with significant hemodynamic changes and vasodilation of the uterine and systemic circulation in order to meet the metabolic demands of the mother and developing fetus. Preeclampsia (PE) is one of the foremost complications of pregnancy and a major cause of maternal and fetal mortality. The pathophysiological mechanisms of PE have been elusive, but some parts of the puzzle have begun to unravel. Genetic factors such as leptin gene polymorphism, environmental and dietary factors such as Ca2+ and vitamin D deficiency, and co-morbidities such as obesity and diabetes may increase the susceptibility of pregnant women to develop PE. An altered maternal immune response may also play a role in the development of PE. Although the pathophysiology of PE is unclear, most studies have implicated inadequate invasion of cytotrophoblasts into the uterine artery, leading to reduced uteroplacental perfusion pressure (RUPP) and placental ischemia/hypoxia. Placental ischemia induces the release of biologically active factors such as growth factor inhibitors, anti-angiogenic factors, inflammatory cytokines, reactive oxygen species, hypoxia-inducible factors, and antibodies to vascular angiotensin II (AngII) receptor. These bioactive factors could cause vascular endotheliosis and consequent increase in vascular resistance and blood pressure, as well as glomerular endotheliosis with consequent proteinuria. The PE-associated vascular endotheliosis could be manifested as decreased vasodilator mediators such as nitric oxide, prostacyclin and hyperpolarizing factor and increased vasoconstrictor mediators such as endothelin-1, AngII and thromboxane A2. PE could also involve enhanced mechanisms of vascular smooth muscle contraction including intracellular Ca2+, and Ca2+ sensitization pathways such as protein kinase C and Rho-kinase. PE-associated changes in the extracellular matrix composition and matrix metalloproteinases activity also promote vascular remodeling and further vasoconstriction in the uterine and systemic circulation. Some of these biologically active factors and vascular mediators have been proposed as biomarkers for early prediction or diagnosis of PE, and as potential targets for prevention or treatment of the disease.

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Women with Preeclampsia Have Higher Plasma Endothelin Levels than Women with Normal Pregnancies

Cited by 51 publications

References 0 publications

Hypertension in Response to Chronic Reductions in Uterine Perfusion in Pregnant Rats

Hypertension in Response to Chronic Reductions in Uterine Perfusion in Pregnant Rats

Resistance Artery Adaptation to Pregnancy Counteracts the Vasoconstricting Influence of Plasma From Normal Pregnant Women

Molecular and Vascular Targets in the Pathogenesis and Management of the Hypertension Associated with Preeclampsia

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