Altered PGE2 production by glomeruli and papilla of rats with hereditary diabetes insipidus.
PGE2 synthesis rate was studied in vitro in isolated glomeruli and in papillary homogenates prepared from kidneys of Brattleboro rats with hereditary diabetes insipidus (DI) (no ADH) and of Brattleboro heterozygous control rats. Incubations were carried out in isotonic buffer at 37 degrees C in the presence or absence of arachidonic acid for 15, 30, 60 and 90 min. PGE2 production was measured in the supernatant by specific radioimmunoassay. Results were compared by analysis of variance. PGE2 production was significantly decreased in the papilla (p < 0.01) and increased in the glomeruli (p < 0.01) of DI rats compared to controls. Stimulation by arachidonic acid was similar in both groups. Chronic ADH deficiency thus modifies the ability of the kidney to produce PGE2 in vitro. The opposite effects observed in glomeruli and papilla suggest a different hormonal control of PGE2 synthesis in both tissues.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D003919:Diabetes Insipidus / Q000235:genetics / Q000378:metabolism*; D005260:Female; D007678:Kidney Glomerulus / Q000378:metabolism*; D007679:Kidney Medulla / Q000378:metabolism*; D008297:Male; D011458:Prostaglandins E / Q000096:biosynthesis*; D051381:Rats; D014667:Vasopressins / Q000502:physiology
D001095:Arachidonic Acids; D011458:Prostaglandins E; D014667:Vasopressins