gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

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Agonistic AT1-Receptor Autoantibodies and Monocyte-Stimulation in Hypertensive Patients

Agonistische AT1-Rezeptor Autoantikörper und Monozyten-Stimulation bei Hypertensiven Patienten

Meeting Abstract (Hypertonie 2004)

Suche in Medline nach

  • Y. Dörffel - Charité - Medizinische Poliklinik (Berlin, D)
  • G. Wallukat - Max-Delbrück-Centrum (Berlin, D)
  • N. Bochnig - Max-Delbrück-Centrum (Berlin, D)
  • M. Herberg - Max-Delbrück-Centrum (Berlin, D)
  • J. Scholze - Charité - Medizinische Poliklinik (Berlin, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP90

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2004/04hoch090.shtml

Veröffentlicht: 10. August 2005

© 2005 Dörffel et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.

Gliederung

Text

Objective: Agonistic AT1-receptor autoantibodies (AT1-AA) have been described in hypertensive and preeclamptic patients. Furthermore, monocytes are activated in hypertensive patients. We investigated the ability of AT1-AA to stimulate monocytes from hypertensive and normotensive persons. The adhesiveness of the monocytes to endothelial cell layers and the tissue factor expression were determined.

Methods: Peripheral blood monocytes from 17 patients with essential hypertension and from 20 normotensive subjects were isolated by Dynabeads and used in adhesion experiments. Adherence assays and Western blotting were done.

Results: Monocyte adhesion to human aortic endothelial cell layers was significantly higher after stimulation with AT1-AA compared to no stimulation. The effect was blocked with tissue factor antibody or epitope peptide preincubation. Eposartan was partially effective in blocking the effects. Western blotting after AT1-AA or Ang II stimulation showed that the monocytes expressed tissue factor.

Conclusion: These data show that monocytes can be stimulated by AT1-AA to adhere and produce tissue factor. They underscore the importance of monocyte activation in hypertensive patients. The relevance of AT1-AA in hypertension will require further studies.