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Acta Physiologica 2009; Volume 195, Supplement 669
The 88th Annual Meeting of The German Physiological Society
3/22/2009-3/25/2009
Giessen, Germany
SYSTEMIC ACTIVATION OF THE RENIN-ANGIOTENSIN SYSTEM CAUSES STIMULATION OF THE INTRAOCULAR RENIN-ANGIOTENSIN SYSTEM
Abstract number: P238
Strauss1 O., Brockmann1 M., Meyer1 C., Todorov2 V., Kurtz2 A., Milenkovic1 V.
1Klinikum der Universitt Regensburg, Experimentelle Ophthalmologie, Klinik und Poliklinik fr Augenheilkunde, Regensburg
2Universitt Regensburg, Institut fr Physiologie, Regensburg
Systemic activation of the renin-angiotensin system serves to prevent a fall in blood pressure and to regulate water and salt balance in the body. Recent evidence showed that there is also an intrinsic renin-angiotensin system active in the retina. The aim of the study was the investigation of a possible influence of the systemic renin-angiotensin system on that of the retina suggesting a cross talk between the kidney and the eye. Using the RT PCR technique we could find angiotensin-receptor-2 in the freshly isolated retina and the retinal pigment epithelial (RPE) cells. This observation could be confirmed by western-blot in which also showed the presence of the angiotensin-receptor proteins. Furthermore, the presence of angiotensin-receptor was found in retinal sections. Calcium measurements performed on the primary culture of the porcine RPE cells confirmed that RPE cells functionally express angiotensin-2 receptors which stimulation leads to an increase in intracellular free Ca2+ as second-messenger. In addition we could show that the systemic decrease in the angiotensin plasma level leads to stimulation of the intraocular renin-angiotensin system. This seems to occur by angiotensin receptors in the RPE which stimulation leads to a decrease the expression of secretable renin. It is very likely that this renin is secreted to the neuronal retina and leads to changes in retinal functions such as neuronal activity and water transport.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 669 :P238