3 patients with Bartter’s syndrome were studied under metabolic ward conditions before and during administration of captopril 25 mg t.i.d. The drug induced an immediate and sustained reduction of blood pressure (by 14 and 18% after 1 h and 3 days, respectively) with no change in heart rate. During treatment renal plasma flow increased by 29%, but the glomerular filtration rate was unchanged. Renal vascular resistance decreased by 41%. There was an increase in urinary sodium excretion with a corresponding reduction of body weight. The potassium balance was not affected. The concentration of angiotensin II became normal but the plasma renin concentration rose tenfold. Plasma renin substrate, initially rather low, was further reduced. The blood pressure responsiveness to angiotensin II increased without being completely normalized. An abnormal production of vasodilating prostaglandins is thought to be an important feature of Bartter’s syndrome. Our findings, notably the marked renal vasodilatation, may reflect the effect of these prostaglandins when unopposed by an increased angiotensin II product