Abstract
An elevated urinary kallikrein excretion was found in 3 out of 4 adult patients with Bartter’s syndrome. After prostaglandin synthesis inhibition by indomethacin, serum potassium levels rose, plasma renin activity and urinary aldosterone excretion decreased. Urinary kallikrein excretion was reduced to within normal range in all patients. The fall of urinary kallikrein excretion after indomethacin may be partly due to plasma potassium and aldosterone variations, but more likely it is dependent on the reduced prostaglandin synthesis. These results support the hypothesis that renal prostaglandins activate renal kallikrein-kinin system, hence inducing an increase of renal blood flow, diuresis and natriuresis.
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Lechi, A., Mantero, F., Opocher, G. et al. Effect of indomethacin on urinary kallikrein excretion in Bartter’s syndrome of the adult. J Endocrinol Invest 4, 17–20 (1981). https://doi.org/10.1007/BF03349408
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DOI: https://doi.org/10.1007/BF03349408