ANGIOTENSIN-II IN THE RABBIT RETINA

We investigated a putative local angiotensin II (AngII) system in the rabbit retina by examining AngII contents in the retina, vitreous humo r, 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 cellu lar 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 AngI I-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 a nd 86 times higher, respectively, than in the plasma. ACE mRNA was pre sent in both retina and choroid. Immunohistochemistry for AngII reveal ed faintly labeled amacrine cells at the inner border of the inner nuc lear layer of the retina. Preincubation with PI resulted in an enhance d immunoreaction and in the labeling of fibers in the inner and outer plexiform layer; Muller cells and their processes as well as ganglion cells were now stained as well but the specificity of ganglion cell st aining remains questionable. The immunoreaction was further enhanced w hen 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 spe cific AngII concentration is maintained there; AngII is localized in d istinct cell types and can be metabolized within these cells. These da ta point to a local retinal AngII system that is protected and indepen dent of blood-borne AngII.