Antidiuretic hormone increases renal prostaglandin synthesis in vivo.
Studies demonstrating the antagonism by prostaglandins (PGs) of antidiuretic hormone (ADH) action led to the proposal that renal medullary PGs may act to attenuate the physiologic effects of ADH via a negative-feedback loop. Therefore, we examined urinary PG excretion, an indicator of renal PG synthesis, in rats with hereditary diabetes insipidus (DI) utilizing gas chromatography-mass spectrometry. The DI rats, devoid of ADH, excrete much less prostaglandin E2 (PGE2) than normal Long-Evans rats (39 +/- 5 vs. 228 +/- 53 ng/24 h, means +/- SE, P less than 0.005). DI and normal rats were treated for 35 days with ADH while separate groups of DI and normal controls received vehicle only. The ADH treatment increased urinary PGE2 excretion in DI rats to 233 +/- 35 ng/24 h whereas PGE2 excretion was unaffected by vehicle treatment. ADH treatment in normal rats similarly increased PGE2 excretion from 215 +/- 49 to 410 +/- 63 ng/24 h (P less than 0.05). To determine whether the rise in PGE2 excretion is the result of the rise in papillary osmolality, we subjected DI rats to dehydration, which increased urine osmolality from 130 +/- 10 to 302 +/- 12 mosmol/kg H2O but left urinary PGE2 unaffected. We conclude that ADH stimulates renal medullary PGE2 synthesis in vivo.
D000818:Animals; D003404:Creatinine / Q000652:urine; D003919:Diabetes Insipidus / Q000235:genetics / Q000652:urine; D007679:Kidney Medulla / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000652:urine; D011458:Prostaglandins E / Q000096:biosynthesis* / Q000652:urine; D051381:Rats; D012964:Sodium / Q000652:urine; D013894:Thirst; D014667:Vasopressins / Q000494:pharmacology*
D011458:Prostaglandins E; D014667:Vasopressins; D012964:Sodium; D003404:Creatinine; D011188:Potassium