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Angiotensin II in the rabbit retina

Published online by Cambridge University Press:  02 June 2009

Konrad Kohler
Affiliation:
Department of Pathophysiology of Vision and Neuroophthalmology, Division of Experimental Ophthalmology, University Eye Hospital, Tübingen, Germany
Thomas Wheeler-Schilling
Affiliation:
Department of Pathophysiology of Vision and Neuroophthalmology, Division of Experimental Ophthalmology, University Eye Hospital, Tübingen, Germany
Bernhard Jurklies
Affiliation:
Department of Pathophysiology of Vision and Neuroophthalmology, Division of Experimental Ophthalmology, University Eye Hospital, Tübingen, Germany
Elke Guenther
Affiliation:
Department of Pathophysiology of Vision and Neuroophthalmology, Division of Experimental Ophthalmology, University Eye Hospital, Tübingen, Germany
Eberhart Zrenner
Affiliation:
Department of Pathophysiology of Vision and Neuroophthalmology, Division of Experimental Ophthalmology, University Eye Hospital, Tübingen, Germany

Abstract

We investigated a putative local angiotensin II (AngII) system in the rabbit retina by examining AngII contents in the retina, vitreous humor, and choroid by radioimmunoassays and AngII synthesis in the retina and choroid by detection of angiotensin converting enzyme (ACE) mRNA. An antibody directed against AngII was used to localize possible cellular sources of AngII in the retina. To enhance immunoreactivity and to further examine AngII metabolism, tissues were preincubated in medium containing either protease inhibitors (PI), PI together with the AngII-precursor AngI, or PI and AngII. In some experiments the conversion of AngI to AngII was blocked by an ACE inhibitor. AngII concentration in the vitreous humor was only about 10% of the plasma concentration; in the retina and the choroid, however, AngII concentrations were 10 and 86 times higher, respectively, than in the plasma. ACE mRNA was present in both retina and choroid. Immunohistochemistry for AngII revealed faintly labeled amacrine cells at the inner border of the inner nuclear layer of the retina. Preincubation with PI resulted in an enhanced immunoreaction and in the labeling of fibers in the inner and outer plexiform layer; Müller cells and their processes as well as ganglion cells were now stained as well but the specificity of ganglion cell staining remains questionable. The immunoreaction was further enhanced when AngI or AngII was added to the incubation medium, whereas labeling totally disappeared when the conversion of AngI to AngII was blocked. No immunoreactive cells were detected in the choroid. In conclusion, the synthesizing enzyme for AngII is expressed in the retina and a specific AngII concentration is maintained there; AngII is localized in distinct cell types and can be metabolized within these cells. These data point to a local retinal AngII system that is protected and independent of blood-borne AngII.

Type
Research Articles
Copyright
Copyright © Cambridge University Press 1997

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