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

Transient receptor potential channel expression in spontaneously hypertensive rats

Transient Receptor Potential Kanäle bei spontan hypertensiven Ratten

Meeting Abstract

  • M. Tepel - Charité - Campus Benjamin Franklin Berlin (Berlin, D)
  • D. Liv - Charité - Campus Benjamin Franklin Berlin (Berlin, D)
  • A. Scholze - Charité - Campus Benjamin Franklin Berlin (Berlin, D)
  • R. Kreutz - Charité - Campus Benjamin Franklin Berlin (Berlin, D)
  • W. Zidek - Charité - Campus Benjamin Franklin Berlin (Berlin, D)
  • Z. Zhu - Department of Hypertension and Endocrinology Chongqing (PR China)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP25

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch025.shtml

Veröffentlicht: 8. August 2006

© 2006 Tepel 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 evaluated the role of calcium-permeable transient receptor potential canonical (TRPC) channel in primary hypertension. TRPC expression in monocytes from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyotot rats (WKY) was determined using in-cell Western assay, and CD14 was used as internal reference. Down-regulation of TRPC3 in cells was perforemd using small interfering RNA (siRNA). Measurements of cytosolic calcium were carried out using the fluorescent dye fura2. The TRPC3/CD14 channel expression was significantly increased in monocytes from SHR compared to WKY (7.7±0.3 vs. 2.9±0.5; mean±SEM; each n=4; p<0.05). On the other hand the TRPC6/CD14 channel expression was not significantly different in SHR compared to WKY (4.3±0.2 vs. 4.7±0.3; each n=4; p=n.s.). After the administration of thapsigargin, an inhibitor of the sarco-endoplasmic calcium-ATPase, the sustained increase of cytosolic calcium was significantly higher in SHR compared to WKY (1.1±0.1 vs. 0.8±0.3; each n=6; p<0.05). Specific TRPC3-knockdown by transfection of monocytes from SHR with siRNA significantly reduced TRPC3 expression, transplasmamembrane calcium influx and thapsigargin-induced sustained calcium increase. The study shows increased TRPC3 channel expression and increased TRPC3-related calcium influx in spontaneously hypertensive rats.