In a patient with Bartter's syndrome (increased plasma renin, juxtaglomerular-cell hyperplasia, hyperaldosteronism and hypokalemia, but no hypertension), aldosterone excretion and secretion were increased only moderately despite marked elevation of plasma renin, presumably because of suppression of aldosterone production by hypokalemia. When the serum potassium was raised by administration of potassium chloride and spironolactone, while normal sodium balance was maintained, aldosterone excretion rose markedly. Infusion of albumin decreased plasma renin and aldosterone secretion, and restored normal sensitivity to the pressor effect of exogenous angiotensin. Suppression of aldosterone production to normal limits by administration of albumin, amino-glutethimide or dexamethasone failed to correct the hypokalemia, indicating that some factor other than hyperaldosteronism may contribute to urinary potassium wastage in this syndrome. This study and others raise the possibility that in some patients with Bartter's syndrome the primary defect is impairment of proximal sodium reabsorption.