The recent discovery of numerous organ specific local renin-angiotensin systems (RAS) has increased the complexity of the classical view of the RAS. The retinal pigment epithelium (RPE) and retina are known to comprise such a system. Its functional implications remain, however, unclear. Regularly, ocular systems are well isolated from systemic influences by the blood-retina barrier, partly built by the RPE. Recent studies have shown an impact of the systemic RAS on the ocular RAS, potentially mediated by the RPE. Furthermore, the use of inhibitors of the systemic RAS, such as angiotensin-converting enzyme (ACE) inhibitors, in the treatment of cardiovascular diseases are known to have unexpected effects on the pathophysiology of namely age-related macular degeneration (AMD). In this context, we investigated both the interplay of the systemic and the local ocular RAS and its implications on eye disease. For this purpose, C57BL/6 mice received different modulators of the systemic RAS. This was achieved by treating the animals with the ACE inhibitor enalapril or the angiotensin II receptor type 1 (AT1) inhibitor losartan in the drinking water (10mg *kg^-1*day^-1) for six days, or by chronic subcutaneous infusions of isoproterenol for three days (10mg *kg^-1*day^-1). After sacrifice, samples of RPE, retinae and kidney were collected and total mRNA was isolated. After reverse transcription, cDNA was further analyzed by real time PCR.

In this study we found an influence of systemic modulation of renin synthesis on its local expression in the intraocular RAS. Through the manipulation of the systemic RAS we also elucidated other target proteins contributing to pro-inflammatory events, ultimately favoring the development of eye disease.