Bartter's syndrome: urinary prostaglandin E-like material and kallikrein; indomethacin effects.
The urinary excretions of prostaglandin E-like material (iPGE) and kallikrein were measured in two children with Bartter's syndrome. Urinary iPGE excretion was three and 10 times greater than normal, and urinary kallikrein was five and 10 times greater than normal in the two subjects. Furthermore, excretions of iPGE and kallikrein were highly correlated (P less than 0.005) with each other before and during treatment with indomethacin, a prostaglandin synthetase inhibitor. Indomethacin significantly (P less than 0.001) reduced urinary iPGE, urinary kallikrein, and plasma renin activity, while increasing the sensitivity to intravenous angiotensin II and the serum potassium to normal. The results confirm that renal prostaglandins may be involved in the pathogenesis of Bartter's syndrome and suggest that renal prostaglandins and the kallikrein-kinin system are linked.
D000450:Aldosterone / Q000652:urine; D000804:Angiotensin II / Q000494:pharmacology; D001477:Bartter Syndrome / Q000652:urine*; D002648:Child; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000652:urine*; D007213:Indomethacin / Q000494:pharmacology*; D007610:Kallikreins / Q000652:urine*; D011458:Prostaglandins E / Q000652:urine*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000652:urine
D011458:Prostaglandins E; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D007610:Kallikreins; D012083:Renin; D007213:Indomethacin