gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Vasoactive peptides in the human placenta: impact on the arachidonic acid signaling

Vasoaktive Peptide in der humanen Plazenta: Einfluß auf die Arachidonsäuresignalübertragung

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker A. Jank - Freie Universität Berlin, Universität Leipzig (Berlin, Leipzig, D)
  • F. Gembardt - Freie Universität Berlin, Universität Leipzig (Berlin, Leipzig, D)
  • H. Stepan - Freie Universität Berlin, Universität Leipzig (Berlin, Leipzig, D)
  • H. Hopp - Freie Universität Berlin, Universität Leipzig (Berlin, Leipzig, D)
  • T. Walther - Freie Universität Berlin, Universität Leipzig (Berlin, Leipzig, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP84

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Jank et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



The placenta is thought to play an important role in the aetiology and pathogenesis of preeclampsia. This clinical syndrome of hypertension, proteinuria and peripheral/cerebral oedema occurs after the 20th week in 3-5% of all pregnancies. The detection of arachidonic acid (AA) release in the placenta observes the basic step in the cyclooxygenase pathway and could offer wide information about the relevance of vasoactive peptides in placental vascular reactivity and inflammation. Therefore the aim of this study was to investigate the role of specific vasoactive peptides for the intracellular signaling in primary human placental cells.

Placental tissue samples of 6 normal and 3 preeclamptic pregnancies at term were prepared for cell culture using a trypsin digestion. 72 hours after first plating the H3-AA-prelabelled placental cells were stimulated by angiotensin II, angiotensin-(1-7), oxytocin and bradykinin (10-10-10-6M) and the AA release was measured.

Preparation of placental tissue for primary cell experiments was successfully established. None of the 4 tested peptides increased the AA release in placental cells of normal pregnancies. Preliminary data with primary placental cells of 3 preeclamptic pregnancies suggest no rise in AA release after stimulation with all tested peptides.

Our data implicate that the tested peptides mediate no enhanced AA release in placental cells. However the measurement of the released AA in primary cell culture of human placenta could be a helpful tool for defining the altered peptide actions in preeclamptic placentas. Further experiments with this assay could identify deregulated signaling for other circulating peptides in placentas with defined pathology.