By W. Burggren, B. Keller
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Additional resources for Devel. of Cardiovascular Systs - Molecules to Organisms
Am. ]. , 237, F20-F24 75. Schnermann, J. e. (1982). Reversal of indomethacin-induced inhibition of tubuloglomerular feedback by prostaglandin infusion. Prostaglandins, 24, 341-36 I 76. L. B. (1984). Relationship between PG and p-adrenergic pathways to renin release in rat renal cortical slices. Am. ]. , 247, E343-E348 77. B. (1979). Effect of prostaglandin E2 on chloride transport across the rabbit thick ascending limb of Henle. ]. CIin. , 64, 495-502 33 3 Arachidonic acid metabolism in renal disease s.
RENAL ARACHIDONIC ACID METABOLISM demonstrating a multiplicity of check points which co-operate to achieve a final effect - viz, the regulation of extracellular fluid volume. Before examining peptide-eicosanoid interactions in mT ALH, a general statement regarding the effects of eicosanoids on the activity of peptide hormones is in order. The concept that prostaglandins and other arachidonate metabolites act locally as either modulators or mediators of peptide hormones and neurotransmitters aids in understanding the multiple and overlapping spheres of biological activity and diverse effects of products of arachidonic acid metabolism 34 .
64, 495-502 33 3 Arachidonic acid metabolism in renal disease s. Lear and V. E. Kelley INTRODUCTION Arachidonic acid (AA) metabolites are produced by a variety of renal cells, although the eicosanoid profile varies among different cell types and regions of the kidney. The details of eicosanoid biosynthesis and metabolism are discussed in a preceding chapter. The importance of arachidonic acid metabolites in renal disease has emerged from experimental studies and clinical evaluation of immunologically mediated, as well as non-immune, forms of renal injury.