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Dergi Kimliği

Online ISSN
1305-3132

Yayın Dönemi
1993 - 2021

Editor-in-Chief
​Cihat Şen, ​Nicola Volpe

Editors
Daniel Rolnik, Mar Gil, Murat Yayla, Oluş Api

New placental vasoactive factors and gestational diseases

E.V Cosmi

Künye

New placental vasoactive factors and gestational diseases. Perinatoloji Dergisi 2002;10(3):162-162

Yazar Bilgileri

E.V Cosmi

  1. University of Rome"La Sapienza" Institute of Gynecology, Perinatology and Child Health Rome IT
Yazışma Adresi

E.V Cosmi, University of Rome"La Sapienza" Institute of Gynecology, Perinatology and Child Health Rome IT,

Yayın Geçmişi
Çıkar Çakışması

Çıkar çakışması bulunmadığı belirtilmiştir.

Recently, among the several hormones and peptides produced by the placental tissues, the role of newly discovered vasoactive factors has been investigated for their involvement in the pathophysiology of gestational diseases. Most of them, besides the effects on vascular system are also implicated in the regulation of other functions such as cellular growth and differentiation, inflammation, smooth muscie cells activity. in this light, we have investigated the potential role of endothelin-1 (ET-1), nitric oxide (NO), and adrenomedullin (AM) in some gestational diseases. ET-1, NO and AM were measured by means of a specific RİA in maternal and tetal plasma and in amniotic fluid and, using an immunohistochemical method, in placental tissues in pregnancy complicated by preeclampsia, IUGR and gestational diabetes. We found that all these vasoactive factors are produced by the placental tissues in large amount and are secreted in the fetal compartment where they participate in the regulation of feto-placental circulation. in pregnancy complicated by preeclampsia. IUGR and gestational diabetes, conditions associaled with impairment of utero-placental and fetal hemodynamics, ET-1, NO and AM secretion is significantly affected. in particular, NO and AM increase significantly in the fetal plasma in response to fetal hypoxia and correlate with the redistribution of fetal cardiac output in response to reduced utero-placental perfusion.
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