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Title: Angiotensin-converting enzyme inhibition as a therapeutic principle in Bartter's syndrome. Author: Jest P, Pedersen KE, Klitgaard NA, Thomsen N, Kjaer K, Simonsen E. Journal: Eur J Clin Pharmacol; 1991; 41(4):303-5. PubMed ID: 1804643. Abstract: The effect of captopril has been investigated in four patients with Bartter's syndrome treated for 12 weeks. Baseline biochemistry showed normal serum aldosterone (mean 347 pmol.l-1) and a mean serum renin of 217 mU-l-1, and a considerable increase in serum renin during captopril treatment. Serum aldosterone decreased gradually during the study period to about half its initial value. The patients presented with a mean serum potassium of 2.5 mmol.l-1, which rose to 3.4 mmol.l-1 on captopril. Lymphocytes showed a substantial captopril-induced increase in intracellular sodium (from 15 to 22.5 mmol.l-1 on average), but no change in the potassium content. Captopril was well-tolerated. It may be an alternative to potassium-sparing diuretics for maintaining normal serum potassium levels in patients with Bartter's syndrome.[Abstract] [Full Text] [Related] [New Search]