Production of potassium depletion by benzothiadiazine compounds ∗

Abstract

Secondary hyperaldosteronism was simulated in seven patients by the administration of desoxycorticosterone acetate (DCA) in doses of 30 mg. per day. In these patients the sodium-retaining properties of this agent appeared to be independent of total exchangeable sodium. The combined administration of hydrochlorothiazide and DCA resulted in a significantly greater kaliuretic effect than that of the sum of the two given separately. Similar results were obtained with other benzothiadiazine compounds. In conditions associated with secondary hyperaldosteronism, i.e., portal cirrhosis with ascites, nephrosis and malignant hypertension, the benzothiadiazine derivatives are likely to produce moderate to severe potassium epletion. Claims that one benzothiadiazine compound causes less potassium depletion than another are meaningless unless endogenous aldosterone secretion is considered.