LARAGH and his co-workers1 have demonstrated that chlorothiazid administered to normal subjects in the midst of a sustained water diuresis provokes a flow of urine of substantially higher concentration for a given rate of total osmolar output than urine formed by water-loaded subjects to whom meralluride is given. On the basis of this finding, they suggested that the site of action of chlorothiazid was in the distal portion of the nephron. Here, they postulated that the drug inhibited the production of ‘free water’ which normally results from selective re-absorption of sodium and accompanying anions. A drug acting to interfere with free-water formation would be of therapeutic value to the patient with diabetes insipidus, particularly the nephrogenic sort, if attendant losses of electrolyte in the urine were not unduly large, or, indeed, should they fail to occur.