Abstract
Endogenous prostaglandin biosynthesis modulates such renal functions as regional blood flow (1), salt and water transport (2), renin secretion (3,4) and neurotransmitter release (5). More recently, the vasoconstrictor thromboxane A2, which normally is quantitatively a minor product of arachidonic acid metabolism in the kidney under resting or basal conditions, has been shown to be increased in several models of renal injury and may be, in part, responsible for some of the pathophysiological derangements (6–9). Two models, ureteral obstruction and subtotal renal ablation, in which thromboxane seems to play a pathogenetic role, are described in more detail in this chapter. In addition, the role of prostaglandins, thromboxane and dietary fatty acids on kidney function and structure in several immunological models of renal disease and hypertension are discussed.
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© 1989 Plenum Press, New York
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Klahr, S., Purkerson, M.L. (1989). Eicosanoids: Role in Experimental Renal Disease. In: Dunn, M.J., Patrono, C., Cinotti, G.A. (eds) Renal Eicosanoids. Advances in Experimental Medicine and Biology, vol 259. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5700-1_11
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