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Abstract. To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal‐sodium diet and four a low‐sodium (17 mmol/day) diet. All patients had a normal initial total body potassium ( 40 K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal‐sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low‐sodium group the highest deficit was 276 mmol on day 13. The normal‐sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low‐sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic‐induced potassium loss, presumably by an increased activity of the renin‐angiotensin‐aldo‐sterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.
LANDMANN‐SUTER et al. (Thu,) studied this question.