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Clin Sci (Lond). 2016 Jul 1;130(13):1075-88. doi: 10.1042/CS20160092. Epub 2016 Mar 29.

Hypertensive retinopathy in a transgenic angiotensin-based model.

Author information

1
Department of Ophthalmology, Charité University Medicine Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.
2
Experimental and Clinical Research Center, a joint co-operation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Lindenberger Weg 80, 13125 Berlin, Germany.
3
Institute of Human Anatomy and Embryology, University of Regensburg, Universitätsstrasse 31, 93053 Regensburg, Germany.
4
Attoquant Diagnostics GmbH, Campus-Vienna-Biocenter 5, 1030 Vienna, Austria.
5
Experimental and Clinical Research Center, a joint co-operation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Lindenberger Weg 80, 13125 Berlin, Germany HELIOS-Klinik Berlin-Buch, Schwanebecker Chaussee 50, 13125 Berlin, Germany.
6
Department of Ophthalmology, Charité University Medicine Berlin, Augustenburger Platz 1, 13353 Berlin, Germany olaf.strauss@charite.de.

Abstract

Severe hypertension destroys eyesight. The RAS (renin-angiotensin system) may contribute to this. This study relied on an established angiotensin, AngII (angiotensin II)-elevated dTGR (double-transgenic rat) model and same-background SD (Sprague-Dawley) rat controls. In dTGRs, plasma levels of AngII were increased. We determined the general retinal phenotype and observed degeneration of ganglion cells that we defined as vascular degeneration. We also inspected relevant gene expression and lastly observed alterations in the outer blood-retinal barrier. We found that both scotopic a-wave and b-wave as well as oscillatory potential amplitude were significantly decreased in dTGRs, compared with SD rat controls. However, the b/a-wave ratio remained unchanged. Fluorescence angiography of the peripheral retina indicated that exudates, or fluorescein leakage, from peripheral vessels were increased in dTGRs compared with controls. Immunohistological analysis of blood vessels in retina whole-mount preparations showed structural alterations in the retina of dTGRs. We then determined the general retinal phenotype. We observed the degeneration of ganglion cells, defined vascular degenerations and finally found differential expression of RAS-related genes and angiogenic genes. We found the expression of both human angiotensinogen and human renin in the hypertensive retina. Although the renin gene expression was not altered, the AngII levels in the retina were increased 4-fold in the dTGR retina compared with that in SD rats, a finding with mechanistic implications. We suggest that alterations in the outer blood-retinal barrier could foster an area of visual-related research based on our findings. Finally, we introduce the dTGR model of retinal disease.

KEYWORDS:

blood–retina barrier; hypertensive retinopathy; renin–angiotensin system; retinal degeneration; vascular damage

PMID:
27026533
DOI:
10.1042/CS20160092
[Indexed for MEDLINE]

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