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

Complement Activation in Angiotensin II-Induced Organ Damage

Meeting Abstract

  • E. Shagdarsuren - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • J.H. Braesen - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • A. Fiebeler - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • R. Dechend - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • P. Gratze - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • F.C. Luft - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • D.N. Muller - Charité - Universitätsmedizin Berlin, Campus Berlin-Buch, Franz-Volhard-Klinik (Berlin, D)
  • M. Wellner - Max-Delbrück-Centrum für Molekulare Medizin (Berlin, D)
  • N. Henke - Max-Delbrück-Centrum für Molekulare Medizin (Berlin, D)
  • J.K. Park - Mediznische Hochschule Hannover (Hannover, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP182

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch182.shtml

Veröffentlicht: 8. August 2006

© 2006 Shagdarsuren 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 vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

We tested whether or not complement activation participates in angiotensin (Ang) II-induced vasculopathy. We used double transgenic rats harboring human renin and angiotensinogen genes (dTGR) with or without losartan (LOS) or the human renin inhibitor aliskiren (ALISK). Sprague-Dawley (SD) rats were controls. DTGR had increased blood pressure at week 5 that increased further by week 7. Albuminuria was absent at week 5, but increased markedly in weeks 6 and 7. CRP elevation, macrophages, T-cells, TNF-a, C1q, C3, C3c, and C5b-9 expression preceded albuminuria. C1q, C3, C3c, and C5b-9 were observed in the dTGR vessel media. C5b-9 co-localized with IL-6. LOS and ALISK reduced albuminuria and complement expression. We also studied vascular smooth muscle cells (VSMC) from dTGR, compared VSMC from SD. C3 and IL-6 mRNA were analyzed after Ang II, TNF-a, and C-reactive protein (CRP) stimulation. VSMC from dTGR showed increased proliferation and C3 expression, compared to SD. Ang II did not induce C3 mRNA in either VSMC type. However, TNF-a and CRP induced C3 mRNA slightly in SD VSMC, but markedly in dTGR VSMC, while IL-6 induction was similar in both. Thus, complement activation and cell infiltration occurred before the onset of albuminuria in Ang II-mediated renal damage. TNF-a and CRP played a major role in C3 activation. VSMC from dTGR are more sensitive for C3 activation. Our data show that in this Ang II-induced model, complement activation is a major participant and suggest that TNF-a and CRP may play a role in its induction.