Summary
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.
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Jest, P., Pedersen, K.E., Klitgaard, N.A. et al. Angiotensin-converting enzyme inhibition as a therapeutic principle in Bartter's syndrome. Eur J Clin Pharmacol 41, 303–305 (1991). https://doi.org/10.1007/BF00314956
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DOI: https://doi.org/10.1007/BF00314956