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The antenatal Bartters syndrome belongs to inherited salt-losing tubulopathies with hypo-kalemic alkalosis. This congenital kidney disease leads to severe fluid and electrolyte distur-bances in the neonate with fatal complications. The elevated level of prostaglandins is charac-teristic for this disease. Many medical and biomolecular trials address to the correlation between the salt-modified setting in the kidney cells and the production of prostaglandins. In the present work I am concerned with the not final resolved way of prostaglandin synthesis. The analysis of the specific cause for the rise of prostaglandins, as well as the involvement of different enzymes, like the cyclooxygenases, the MAP kinases and proteinkinase C is in the focus of my work. Thereby, I worked with an experimental cell model of primary cultivated kidney epithelial cells. By stimulating the cells with different types of salt medias and by adding specific en-zyme inhibitors I analysed the expression of cyclooxygenases on the RNA level as well as the prostaglandin E2 synthesis by ELISA test. Kidney epithelial cells in native state produce only a rare amount of prostaglandins. By incubating the cells in a hypoosmolaric medium an 70-fold rise of PGE2 was demon-strated. The central role of chloride as an adequate stimulus for the PGE2 synthesis could not be proved. The question, which cyclooxygenase has more influence on the production of PGE2, could not be clarified finally in the present examination. Though the mRNA results demonstrated an increased expression of COX-2, it was not possible to detect an exclusive in-volvement of COX-2 by analysing the PGE2 values by ELISA test. The examinations with the enzyme inhibitors of MAP kinases and proteinkinase C foreshadow an involvement of both enzyme groups in the expression of COX-2 and the PGE2 synthesis. In the course of this work the suitability of the present used cell model for the clarification of the outlined questions was revealed.