Prostaglandins and the developing kidney.
Prostaglandins PGE2, PGD2, PGI2, and PGF2 alpha, as well as thromboxanes and leukotrienes, are synthesized by the fetal and neonatal kidney. The major prostaglandin, PGE2, PGD2, and PGI2, increase RBF, free water clearance, urine flow, and natriuresis. Alterations in the synthetic and catabolic activity of renal prostaglandins with advancing gestational and postnatal age occur along with concomitant alterations in RBF, GFR, and water and electrolyte excretion, suggesting that the prostaglandins play an important role in renal functional development. Indomethacin treatment may affect both fetal and neonatal renal function. Long-term maternal indomethacin treatment may decrease fetal urine output enough to alter amniotic fluid volume. Neonatal indomethacin therapy may cause transient dose-related renal dysfunction characterized by a decrease in urine output, but this renal dysfunction also depends in part on dosage, timing of therapy, and the cardiovascular and renal status of the infant prior to treatment. New areas of research interest include urinary prostaglandins as a marker for development of essential hypertension, and the possible interaction between antenatal steroids and renal function in the newborn.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001834:Body Water / Q000378:metabolism; D005919:Glomerular Filtration Rate; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007231:Infant, Newborn; D007234:Infant, Premature; D007668:Kidney / Q000196:embryology / Q000254:growth & development*; D011453:Prostaglandins / Q000096:biosynthesis / Q000502:physiology*; D012039:Regional Blood Flow; D012965:Sodium Chloride / Q000652:urine
D001095:Arachidonic Acids; D011453:Prostaglandins; D016718:Arachidonic Acid; D012965:Sodium Chloride; D007213:Indomethacin