Thromboxane A<sub>2</sub> synthesis in pregnancy‐induced hypertension

Dj, Fitzgerald; Rocki, W; Murray, Rosemary; Mayo, Gail; Ga, FitzGerald

doi:10.1016/0020-7292(91)90552-g

Cited by 27 publications

(34 citation statements)

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“…Thus, increased TXA2 biosynthesis appears to correlate with the severity of PE and may have a pathogenetic role in the disease. These findings have provided a rationale for using aspirin in treatment/prevention of PE (Fitzgerald, 1990). Some studies have suggested that low dose aspirin may attenuate the development of PE in women at risk for the disease (Coomarasamy, 2001).…”

Section: Role Of Txa2 In Pementioning

confidence: 95%

Neurovascular Mechanisms of Hypertension in Pregnancy

Stennett

Khalil²

2006

CNR

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Normal pregnancy is associated with significant changes in the neuronal and vascular control mechanisms of blood pressure (BP). Preeclampsia (PE) is a major complication of pregnancy characterized by proteinuria, and increased vascular resistance and BP. If untreated, PE leads to eclampsia with serious seizures and severe hypertension. However, the neurovascular mechanisms of hypertension in pregnancy and PE are unclear. Studies in animal models of hypertension in pregnancy suggest that inadequate cytotrophoblast invasion of uterine spiral arteries causes reduction in uteroplacental perfusion pressure leading to placental ischemia/hypoxia. Placental ischemia may promote the release of biologically active factors such as cytokines and reactive oxygen species. These circulating factors may increase the vascular permeability, cross the blood-brain barrier, and affect the sympathetic tone and the neuronal control mechanisms of BP. Placental factors could also cause endothelial cell dysfunction and inhibit nitric oxide (NO)-cyclic guanosine monophosphate (cGMP), prostacyclin (PGI(2))-cyclic adenosine monophosphate (cAMP), and hyperpolarizing factor vascular relaxation pathways. Additionally, placental factors may induce endothelium-derived contracting factors such as endothelin, thromboxane and angiotensin II, which stimulate Ca(2+)-dependent vascular smooth muscle (VSM) contraction or increase protein kinase C activity and enhance myofilament sensitivity to intracellular free calcium concentration ([Ca(2+)](i)). The increased sympathetic tone combined with systemic decrease in endothelium-dependent vascular relaxation and enhanced VSM contraction may contribute to the increased vascular resistance and BP associated with PE. The hypertensive state in severe PE may weaken the blood-brain barrier and precipitate convulsions and cerebral hemorrhage. Careful monitoring of maternal neuronal, endothelial, and VSM function during pregnancy should circumvent the life-threatening neurovascular complications of PE-eclampsia.

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Section: Role Of Txa2 In Pementioning

confidence: 95%

Neurovascular Mechanisms of Hypertension in Pregnancy

Stennett

Khalil²

2006

CNR

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“…The pathogenesis of HELLP syndrome is unclear but an imbalance of prostacyclin and thromboxane has been suggested [18,19]. Patients with HELLP syndrome typically have evidence of preeclampsia as well as thrombocytopenia.…”

Section: Pregnancy-related Liver Disease: Is There Ever An Indicationmentioning

confidence: 98%

Pregnancy and sexual function in liver transplantation

Heneghan

Selzner

Yoshida

et al. 2008

Journal of Hepatology

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“…Preeclampsia has been shown to be associated with an increase in the sympathetic activity [47]. Thromboxane A2 synthesis, as measured by urinary excretion of thromboxane B2 metabolites, has been demonstrated to be significantly higher in patients with pregnancy-induced hypertension [48]. It has been suggested that the ratio of thromboxane A2 to prostacyclin may be higher in preeclampsia, whereas the absolute concentrations may not be different [49].…”

Section: Circulating Parameters In Vascular Maladaptationmentioning

confidence: 99%

The role of RAS in the pathogenesis of preeclampsia

Shah

2006

Current Science Inc

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Preeclampsia is a hypertensive disorder that is unique to pregnancy, with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression in human preeclampsia and in transgenic mouse models with a human preeclampsia-like syndrome shows that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. Vascular maladaptation in preeclampsia with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms through angiotensin receptor type I (AT1) activation. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1 and bradykinin B2 receptor heterodimerization and the production of autoantibody against AT1. Various organ systems with predilection for involvement in preeclampsia are sites of tissue-based RAS. Angiotensin II-mediated mechanisms may explain the primary clinicopathologic features of preeclampsia. In this review, these various aspects are critically examined and an integrated concept on the role of RAS in preeclampsia is presented.

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Thromboxane A₂ synthesis in pregnancy‐induced hypertension

Cited by 27 publications

References 0 publications

Neurovascular Mechanisms of Hypertension in Pregnancy

Neurovascular Mechanisms of Hypertension in Pregnancy

Pregnancy and sexual function in liver transplantation

The role of RAS in the pathogenesis of preeclampsia

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Thromboxane A2 synthesis in pregnancy‐induced hypertension

Cited by 27 publications

References 0 publications

Neurovascular Mechanisms of Hypertension in Pregnancy

Neurovascular Mechanisms of Hypertension in Pregnancy

Pregnancy and sexual function in liver transplantation

The role of RAS in the pathogenesis of preeclampsia

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Thromboxane A₂ synthesis in pregnancy‐induced hypertension