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Olaf Strauss, Rene Barro-Soria, Vladimir Todorov, Frank Schweda, Vladimir V. Milenkovic; Systemic Modulation Of Intraocular Renin/angiotensin System By Renin Expression In The Rpe. Invest. Ophthalmol. Vis. Sci. 2011;52(14):876.
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© ARVO (1962-2015); The Authors (2016-present)
The retina expresses a local renin-angiotensin system (RAS) which is possibly linked to the systemic RAS. An understanding of the systemic modulation of the intra-ocular RAS could help to explain systemic influences in retinal degeneration such as diabetic retinopathy or age-related macular degeneration. The aim of this study is to investigate the systemic influence on renin synthesis, the expression of renin and the underlying Ca2+ signalling in the retinal pigment epithelium (RPE).
qPCR for renin in the mouse kidney and retina; RIA measurement of renin activity in the retina; Ca2+ imaging of short-time cultured procine RPE cells, influence on systemic RAS: water deprivation, enalapril administration, AngII infusion, immunocytochemistry, Ca2+ imaging.
Freshly isolated RPE cells showed expression of secreted isoform renin 1A. The systemic administration of ACE inhibitor enalapril increased the renin expression in both the mouse kidney and retina. Under these conditions the presence of renin protein could be shown by immunhistochemistry and renin activity in the retina could be measured by RIA. In contrast, systemic infusion of AngII decreased in the renin expression in the kidney and in the retina. Water deprivation led to an increase of the renin expression in the kidney but unexpectedly to a decrease of the renin expression in the retina. The mouse retina expresses the AngII receptor AT1 which was found in the RPE and localized at the blood side of the epithelium but also in the inner retina in ganglion cells. Short-time cultured RPE cells responded with increases in intracellular free Ca2+ to stimulation by AngII.
In summary we conclude that the renin expression in RPE cells which form part of the blood/retina barrier is influenced by the systemic RAS. It is likely that AngII circulating in the plasma is a mediator of this influence.
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