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Laragh, Heinemann, and Demartini first reported that the administration of chlorothiazide during water diuresis results in an increased rate of solute excretion without significant changes in the rate of urine flow (1, 2). This effect was interpreted as indicating that the drug interferes with solute (sodium) reabsorption in the distal portions of the nephron where urinary dilution occurs. Similar evidence supporting the concept that chlorothiazide impairs sodium reabsorption at diluting sites in the distal convolution has been presented elsewhere (3). Such a site of inhibition of sodium reabsorption readily accounts for the increased urinary osmolality observed when thiazide derivatives are administered acutely.' Crawford and Kennedy, however, observed that the chronic administration of thiazide derivatives to animals with pituitary diabetes insipidus, and to patients with pituitary or nephrogenic diabetes insipidus, results in a striking diminution in urinary volume as well as an increased urinary osmolality (5). The latter observations have been

THE MECHANISM OF ANTIDIURESIS ASSOCIATED WITH THE ADMINISTRATION OF HYDROCHLOROTHIAZIDE TO PATIENTS WITH VASOPRESSIN-RESISTANT DIABETES INSIPIDUS*