Disease relevance of Hypertension, Pregnancy-Induced

• We conclude that low daily doses of aspirin taken during the third trimester of pregnancy significantly reduce the incidence of pregnancy-induced hypertension and pre-eclamptic toxemia in women at high risk for these disorders, possibly through the correction of an imbalance between levels of thromboxane and prostacyclin [1].
• The possibility of preventing pregnancy-induced hypertension (PIH) and pre-eclampsia in primigravidae by suppressing production of thromboxane A2 with low-dose aspirin was investigated in a randomised, placebo-controlled, double-blind trial [2].
• H-Aogen has been quantitated in plasma from normotensive menstruating women, estrogen treated women, normotensive pregnant women, women with pregnancy-induced hypertension (PIH), and women whose preexisting hypertension was exacerbated during pregnancy [3].
• RESULTS: The IVF mothers had more pregnancy-induced hypertension (21% vs 4%), premature labor (44% vs 22%), labor induction (25% vs 1%), and preterm delivery (37% vs 21%) [4].
• The effects of 3g eicosapentaenoic acid daily on recurrence of intrauterine growth retardation and pregnancy induced hypertension [5].

High impact information on Hypertension, Pregnancy-Induced

• Plasma endothelin-1 levels in patients with pregnancy-induced hypertension [6].
• Effect of low-dose aspirin on fetal and maternal generation of thromboxane by platelets in women at risk for pregnancy-induced hypertension [7].
• We performed a randomized study of the effect of the long-term daily administration of 60 mg of aspirin (n = 17) or placebo (n = 16) on platelet thromboxane A2 and vascular prostacyclin in women at risk for pregnancy-induced hypertension [7].
• We carried out a prospective, randomized, double-blind, placebo-controlled study to investigate the capacity of aspirin to prevent pregnancy-induced hypertension and to alter prostaglandin metabolism [1].
• Excretion of both 2,3-dinor-TxB2 (median 3919, range 683-16,680 pg/mg creatinine) and 11-dehydro-TxB2 (median 10,187, range 434-57,203 pg/mg creatinine) was significantly higher in the patients with pregnancy-induced hypertension than in the normotensive pregnant group (927[273-1343] and 774[500-2760] pg/mg creatinine, respectively) [8].

Chemical compound and disease context of Hypertension, Pregnancy-Induced

• Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae [2].
• Thromboxane metabolite excretion correlated with mean arterial blood pressure, plasma lactate dehydrogenase, and platelet count which are indices of the severity of pregnancy-induced hypertension [8].
• Enalapril and pregnancy-induced hypertension [9].
• Endogenous biosynthesis of arachidonic acid epoxides in humans: increased formation in pregnancy-induced hypertension [10].
• To examine the role of mineralocorticoids in the pathophysiology of pregnancy-induced hypertension (PIH), we studied plasma aldosterone and 18-hydroxycorticosterone levels in 25 women with PIH and 25 normal pregnant women, as controls [11].

Biological context of Hypertension, Pregnancy-Induced

• 0. The frequency of HLA DR4 was higher in sisters with pregnancy-induced hypertension than in sisters with normotensive pregnancies (8/18 [44%] vs 10/54 [19%]) and more of them shared HLA DR4 with their spouses (4/14 [29%] vs 0/29) [12].
• Gestational hypertension is associated with insulin-resistance; insulin and insulin-like growth factor-1 (IGF-1), acting through their receptors, play a role in the growth of the feto-placental unit [13].
• The changes in the amount and activity of vascular PKC isoforms may, in part, explain the changes in vascular resistance during normal pregnancy and pregnancy-induced hypertension [14].
• Alteration of the adrenomedullin receptor components gene expression associated with the blood pressure in pregnancy-induced hypertension [15].
• 4. Women with established pregnancy-induced hypertension had a more rapid Evans Blue disappearance rate and a lower plasma volume than normal pregnant women, independent of the presence of proteinuria [16].

Anatomical context of Hypertension, Pregnancy-Induced

• We have previously found that the relation between Ca(2+) entry and the developed force in vascular smooth muscle is altered during normal pregnancy and in a rat model of pregnancy-induced hypertension produced by long-term treatment with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) [14].
• Sodium pump numbers and cation transport of lymphocytes in pregnancy-induced hypertension [17].
• Marked elevations in plasma thromboxane levels during ovine pregnancy-induced hypertension may have had an "exhaustive" effect on thrombocytes which was reversed by thromboxane synthetase inhibition [18].
• OBJECTIVES: To estimate the cord blood levels of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in preterm infants and to study the relationship of these levels to pregnancy-induced hypertension (PIH) and absolute neutrophil counts [19].
• Erythrocyte morphologic features and serum chemistry studies in ovine pregnancy-induced hypertension treated with thromboxane synthetase inhibitors [20].

Gene context of Hypertension, Pregnancy-Induced

• This study tests the hypothesis that abnormalities in plasma indices of angiogenesis, such as Vascular Endothelial Growth Factor (VEGF) and angiopoietins (Ang-1, Ang-2), as well as their soluble receptors Flt-1 (sFlt-1) and Tie 2 (sTie-2) respectively, are present in women with in pregnancy-induced hypertension (PIH) [21].
• Placental expression of cytokeratin 18 and serum levels of tissue polypeptide antigen in women with pregnancy-induced hypertension [22].
• Some investigators suggested the effect of catechol estrogen on human placental steroidogenesis which may be related to pregnancy-induced hypertension (PIH) through the inhibition of catechol-O-methyltransferase (COMT) activity [23].
• To test this hypothesis, we measured plasma levels of immunoreactive tumor necrosis factor (TNF)-alpha and -beta, interleukin (IL)-1 alpha and -beta, and IL-6 and -10 in women with preeclampsia, in women with transient gestational hypertension, and throughout normal pregnancy [24].
• Our data indicate that the expression of ICAM-1 and PECAM-1 is upregulated in patients with pregnancy-induced hypertension [25].

Analytical, diagnostic and therapeutic context of Hypertension, Pregnancy-Induced

• In a previous longitudinal study of urinary kallikrein (UK) excretion in pregnancy we reported that women with low inactive UK (IUK) to creatinine ratio (IUK:Cr), measured at 16-20 weeks gestation, were at increased risk of developing pregnancy induced hypertension [26].
• Plasma ANP levels were significantly higher in the pregnancy-induced hypertension patients than in the control group [27].
• METHODS: Alpha-tocopherol serum levels were determined by high-pressure liquid chromatography in 177 third-trimester pregnant women: 63 affected by gestational hypertension, 69 by preeclampsia, 26 by chronic hypertension, and 19 normotensive controls [28].
• The influence of pregnancy-induced hypertension (pre-eclampsia) on muscarinic cholinergic receptors and on acetylcholinesterase (AChE) activity was investigated using frozen sections of the umbilical artery and vein [29].
• Adrenomedullin concentrations in plasma from women with normotensive pregnancies, gestational hypertension, and preeclampsia were determined by radioimmunoassay [30].

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