gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Influence of monocyte adhesion and activation by telmisartan

Einfluß von Telmisartan auf Adhäsivität und Aktivierungszustand von Monozyten

Meeting Abstract

  • A. Moebes - Charité - Universitätsmedizin Berlin (Berlin, D)
  • J. Scholze - Charité - Universitätsmedizin Berlin (Berlin, D)
  • Y. Dörffel - Charité - Universitätsmedizin Berlin (Berlin, D)
  • U. Syrbe - Deutsches Rheumaforschungszentrum Berlin (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP79

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

Published: August 8, 2006

© 2006 Moebes 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.



Circulating monocytes from hypertensive patients show elevated secretion patterns of proinflammatory cytokines, an increased expression of adhesion molecules, and an increased adhesion to vascular endothelial cells. We tested the hypothesis that telmisartan, an AT1 receptor antagonist, reduces the activation of circulating monocytes from hypertensive patients and diminishes the monocyte-endothelial cell adhesion. Blood samples were obtained from 20 hypertensive patients before any drug administration and after antihypertensive therapy with telmisartan for three months.Circulating blood monocytes were isolated by density gradient centrifugation and Dynabeads and used in adhesion experiments with human aortic endothelial cells. We assessed the CD11a/b, CD54, CD80, CD86, CCR1 and CCR5 expression using flow cytometry. Telmisartan therapy reduces significantly (P=0,02) the monocyte adhesion to endothelial cell monolayers. Monocyte adhesion after stimulation with angiotensin II was significantly increased before telmisartan therapy but showed no response after therapy. The expression of CD11a/b, CD54, and CCR5 were significantly increased after telmisartan therapy. The AT1 receptor antagonist telmisartan diminished significantly the adhesion of circulating monocytes to human endothelial cells. Reduced monocyte adhesion by telmisartan may be a novel therapeutic approach to prevent vascular alterations in hypertension. The relevance of CD11a/b, CD54, CCR1, and CCR5 in monocyte adhesion will require further studies.