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CF Arndt, C Knauf, G Caputo, J-C Beauvillain, R Matran; Cellular Effects of Corticosteroids on the Retinal Pigment Epithelium . Invest. Ophthalmol. Vis. Sci. 2002;43(13):714.
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Purpose:Central serous chorioretinopathy (CSRC) has been linked to corticosteroid treatment. Previously, an electrophysiological effect compatible with impaired apical (subretinal) fluid absorption has been shown. However the precise mechanisms of these findings remain to be demonstrated. Methods:In bovine RPE choroid preparations, the effect of pretreatment with either apical brimonidine (n=8), SQ 22365 (a specific inhibitor of adenylate cyclase) (n=7) or sodium nitroprusside (SNP), a nitric oxide (NO) donor (n=6) before applying apical hydrocortisone (HC) was compared with the response to HC only. In a similar manner, the response to free HC was compared to HC attached to bovine serum albumine (BSA). The preparations were compared 2 by 2, each pair was obtained from the same eye, in the same conditions. Western blot techniques were employed to detect the presence of nitric oxide synthetase (NOS). Basal NO production was measured in the RPE-choroid preparations. Results:The response to HC was significantly reduced after pretreatment by either brimonidine, SQ 22365 or SNP. The response to HC and HC-BSA was similar, although the effect was retarded with the HC-BSA preparation. The presence of endothelial NOS in RPE preparations could be identified. However no basal NO production was detected. Conclusion:The electrophysiological effects related to HC are probably related to the existence of an apical membrane receptor to corticosteroids. The cellular effect is probably mediated by increased cellular AMPc levels. NO might have a protective effect explaining why CRSC does not occur more often in case of systemic treatment with corticosteroids.
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