gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Non congruent signaling of Angiotensin II and the autoantibody against the AT1 receptor

Nicht kongruentes Signaling von Angiotensin II und dem Autoantikoerper gegen den AT1 Rezeptor

Meeting Abstract (Hypertonie 2004)

Suche in Medline nach

  • presenting/speaker A. Heiss - Charité Berlin - Campus Benjamin Franklin (Berlin, D)
  • presenting/speaker F. Gembardt - Charité Berlin - Campus Benjamin Franklin (Berlin, D)
  • presenting/speaker J. Zhang - Erasmus Medical Center (Rotterdam, NL)
  • presenting/speaker T. Walther - Erasmus Medical Center (Rotterdam, NL)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP43

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Veröffentlicht: 10. August 2005

© 2005 Heiss et al.
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Preeclampsia is a serious health care problem, affecting 4% to 8% of all pregnancies worldwide. Preeclampsia is a specific form of gestational blood pressure elevation combined with proteinuria usually occurring after week 20 of gestation. Recent evidence is indicating that preeclampsia is associated with the presence of agonistic autoantibodies (AT1-AA) in the plasma of these patients, capable to activate the angiotensin (Ang) II receptor AT1. We firstly investigated the [3H]arachidonic acid (AA) release in human trophoblasts of normotensive pregnancies after stimulation with Ang II, AT1-AA or in combination of both. In primary trophoblast culture, neither Ang II (1.2fold), AT1-AA (1.1fold), nor the combination of both (1.1fold) could increase the AA-release in comparison to unstimulated cells. Since activator protein-1 (AP1) transcription factor is discussed to play an important role in apoptosis and inflammation, which are stimulated in preeclampsia, we furthermore investigated the capability of Ang II and AT1-AA to stimulate AT1 receptor-mediated activation of AP1. HEK293 cells, transfected with a plasmid containing the AT1 cDNA, driven by a CMV promoter, were used for dual luciferase assays. For measurements cells were co-transfected with plasmids encoding firefly-luciferase driven by an AP1- induced promoter and a plasmid encoding renilla-luciferase, which was used as an internal control. Cells were stimulated with Ang II, AT1-AA or in combination of both. AT1-AA could not significantly increase the luciferase activity of AP1 via the AT1 (1.24fold) compared with baseline, whereas Ang II (17.44fold) could. Combined stimulation of Ang II and AT1-AA could not exceed luciferase activity (11.46fold). Our results indicate, that the AT1-AA has not per se agonistic properties. Thus a pathophysiological preconditioning, as in preeclampsia, is required for the AT1-AA to process its stimulatory effects of the AT1 mediated signaling pathways.