Lack of evidence for a role for prostaglandins in the mediation of impaired urinary concentrating ability in Bartter's syndrome.
Imparied urinary concentrating ability in Bartter's syndrome may result in part from overproduction of prostaglandins and from the defect in chloride reabsorption by the loop of Henle, or both. To assess the role of prostaglandins, concentration of the urine before and after treatment with prostaglandin inhibitors was studied in 3 patients with this syndrome, taking a constant metabolic diet. Maximal urinary osmolality was determined after overnight fluid deprivation and during infusion of Pitressin. The studies were repeated after 4 days of treatment with the prostaglandin inhibitors, indomethacin and ibuprofen. The maximal urinary osmolality was 694 +/- 39 and 717 +/- 78 mosm/kg, and solute clearance was 1.3 +/- 0.3 and 1.2 +/- 0.5 ml/min for the control and treatment periods, respectively. Prostaglandin inhibitors failed to increase the maximal urinary osmolality or solute clearance. The data thus suggest that factors other than prostaglandin overproduction cause the impairment in urinary concentration in Bartter's syndrome. The defective chloride transport with a loss of interstitial hyperosmolality may be one such factor.
D000293:Adolescent; D001477:Bartter Syndrome / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology*; D007052:Ibuprofen; D007213:Indomethacin; D007671:Kidney Concentrating Ability; D008875:Middle Aged; D009994:Osmolar Concentration; D011188:Potassium / Q000097:blood; D011453:Prostaglandins / Q000502:physiology*; D014556:Urine
D011453:Prostaglandins; D011188:Potassium; D007052:Ibuprofen; D007213:Indomethacin