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pubmed-article:8955502pubmed:dateCreated1997-3-20lld:pubmed
pubmed-article:8955502pubmed:abstractTextEndothelin-1 (ET-1) is a potent vasoconstrictor released by vascular endothelium. Because endothelial cell damage is considered determinant in the pathophysiology of pregnancy-induced hypertension (PIH), this study was conducted to evaluate the role of ET-1 produced by feto-placental tissues in PIH. Amniotic fluid samples obtained by amniocentesis from patients with PIH (N = 33), intrauterine growth retardation (IUGR) (N = 16), and PIH associated with IUGR (N = 12) were evaluated for ET-1 and compared to 42 normotensive pregnancies using a specific radioimmunoassay. ET-1 levels were significantly increased in PIH (35.6 +/- 1.9 pg/ml) and IUGR groups (33.8 +/- 4.6 pg/ml) compared to controls (20.8 +/- 1.4 pg/ml) (P < 0.01). In patients with PIH associated with IUGR, ET-1 concentrations were higher (P < 0.05) with no correlation with the severity of IUGR. Our data indicate that in PIH and IUGR ET-1 production and/or secretion is enhanced in the amniotic compartment, suggesting that the peptide may contribute to the pathophysiologic modification observed in these conditions.lld:pubmed
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pubmed-article:8955502pubmed:monthNovlld:pubmed
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pubmed-article:8955502pubmed:authorpubmed-author:CosmiE VEVlld:pubmed
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pubmed-article:8955502pubmed:authorpubmed-author:Di IorioRRlld:pubmed
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pubmed-article:8955502pubmed:volume36lld:pubmed
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pubmed-article:8955502pubmed:pagination260-3lld:pubmed
pubmed-article:8955502pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:8955502pubmed:year1996lld:pubmed
pubmed-article:8955502pubmed:articleTitleAmniotic fluid endothelin-1 levels are increased in pregnancy-induced hypertension and intrauterine growth retardation.lld:pubmed
pubmed-article:8955502pubmed:affiliation2nd Department of Obstetrics and Gynecology, University La Sapienza, Rome, Italy.lld:pubmed
pubmed-article:8955502pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8955502pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed