Abstract
Three patients with Bartter''s syndrome were studied under metabolic ward conditions before and during administration of captopril 25 mg 3 times daily. 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 Na excretion with a corresponding reduction of body weight. The K balance was not affected. The concentration of angiotensin II became normal but the plasma renin concentration rose 10-fold. 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 (PG) is thought to be an important feature of Bartter''s syndrome. The findings, notably the marked renal vasodilation, may reflect the effect of these PG when unopposed by an increased angiotensin II production.