Abstract
The biosynthetic capacity of the mammalian kidney to produce prostaglandins is exceeded only by the seminal vesicles. Although the medulla is the major site of synthesis in the kidney, an appreciable and physiologically important synthesis also occurs in the glomeruli, arterioles and collecting ducts. Aspirin and the nonsteroidal anti-inflammatory (NSAI) agents are potent inhibitors of prostaglandin synthase1,2. Vane1 suggested that most of the side effects produced by this class of drugs were a consequence of the decreased tissue production of specific prostaglandins, which normally exerted protective effects3. It has since been assumed that the renal toxicity of NSAIs arises from the inhibition of renal prostaglandin production. Accordingly, renal prostaglandins should also protect the kidney from the effects of non-NSAI drug or disease-induced renal damage. In recent years other metabolites of arachidonic acid have been discovered with a wide range of biological activities. The diversity of products complicates our understanding of their role in renal function, especially when we try to explore their role in nephrotoxicity. In this chapter our present understanding of the function of the renal prostaglandins will be reviewed, and related to various animal models of nephrotoxicity and human renal disease.
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Crowshaw, K. (1987). Prostaglandins and Other Eicosanoids. In: Bach, P.H., Lock, E.A. (eds) Nephrotoxicity in the experimental and clinical situation. Developments in Nephrology, vol 19-20. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3367-5_11
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DOI: https://doi.org/10.1007/978-94-009-3367-5_11
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