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

Target organ damage of the eyes in Stroke-Prone Spontaneously Hypertensive Rats (SHRSP)

Endorganschädigung der Augen im spontan hypertensiven Rattenmodell SHRSP

Meeting Abstract

Suche in Medline nach

  • M. Huber - Institut für Klinische Pharmakologie und Toxikologie der Charité ( Berlin, D)
  • M. Wehland - Institut für Klinische Pharmakologie und Toxikologie der Charité ( Berlin, D)
  • R. Kreutz - Institut für Klinische Pharmakologie und Toxikologie der Charité ( Berlin, D)
  • M. Shakibaei - Institut für Anatomie der Charité Berlin

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP37

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch037.shtml

Veröffentlicht: 8. August 2006

© 2006 Huber 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

Introduction: Although target organ damage of the eyes is a frequent clinical complication of hypertension the underlying mechanisms are still unclear. Therefore the aim of this study was to characterize in SHRSP hypertensive effects on the eyes at the morphological and molecular level with the focus on the expression of the nitric oxide synthase isoforms.

Methods: We studied male adult SHRSP with established hypertension at 4 and 12 months of age in comparison to the normotensive WKY controls (n=10-20).

The eyes were dissected by microsurgery for expression and morphological analysis. The mRNA expression of the inducible, neuronal and endothelial nitric oxide synthase isoforms (iNOS, nNOS, eNOS) were quantified in triplicate by Realtime PCR using an ABI PRISM 7000 Sequence Detection System. Light and electron microscopy were carried out according to standard procedures.

Results: In 4 months old SHRSP animals iNOS and nNOS are significantly higher expressed (p<0.05) compared to WKY, whereas eNOS differs not significantly (p>0.05). This is paralleled by morphological changes showing widened microvessels of the ciliary body and degenerative capillaries in the retina.

In 12 months old SHRSP the expression of iNOS is significantly decreased (p<0.05), while the expressions of nNOS and eNOS are similar compared to WKY (p>0.05). At this age the choroideal vessels are enlarged and the neuronal outer nuclear layer is thinner in SHRSP compared to WKY.

Discussion: The degenerative changes in SHRSP illustrate target organ damage of the eyes, which is not restricted to the microvasculature but proceeds to neuronal degeneration. During initial target organ damage the nitric oxide synthase isoforms iNOS and nNOS are highly upregulated probably as a reaction on an impaired microcirculation. This response is lost during further progress of the disease.