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Bartter's Syndrome: Urinary Prostaglandin E-like Material and Kallikrein; Indomethacin Effects
- PERRY V. HALUSHKA, M.D., Ph.D.;
- HULDA WOHLTMANN, M.D.;
- PHILIP J. PRIVITERA, Ph.D.;
- GILBERT HURWITZ, M.D.; and
- HARRY S. MARGOLIUS, M.D., Ph.D.
Abstract
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 < 0.005) with each other before and during treatment with indomethacin, a prostaglandin synthetase inhibitor. Indomethacin significantly (P < 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.
Article and Author Information
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▸From the Departments of Basic and Clinical Pharmacology, Medicine, and Pediatrics, Medical University of South Carolina; Charleston, South Carolina.
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Grant support: by Grants GM20387 and HL17705. Dr. Halushka is a recipient of a Pharmaceutical Manufacturers Association Foundation Faculty Development Award in Clinical Pharmacology. Dr. Margolius is a Burroughs Wellcome Scholar in Clinical Pharmacology.
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▸Requests for reprints should be addressed to Perry V. Haluska, M.D., Ph.D.; Department of Basic and Clinical Pharmacology; Medical University of South Carolina; 80 Barre Street; Charleston, SC 29401.
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- Received November 3, 1976.
- Accepted March 9, 1977.
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