THE MECHANISMS by which diuretics exert their effects are probably as various as the drugs themselves. Thus, mercurials have been shown to have direct, nonhemodynamic, effects on the convoluted tubules of the kidney, interfering with reabsorption of chloride, sodium, and, consequently, water. Potassium excretion after mercurials depends more upon body stores, and it is increased by high water and low sodium (reabsorption competition) loads. Moreover, if energy, released perhaps by breakdown of high-energy phosphate bonds, is required for renal tubular reabsorption, inhibition of the activities of enzymes such as adenosine triphasphatase 1 and succinic dehydrogenase 2 shown by mercurials may help to explain their effect. Histochemically, this inhibition has even been localized in the proximal convoluted tubules,3 although the obligatory energized reabsorption presumably occurs in the distal tubules Xanthine, e. g., aminophylline, diuresis parallels and augments that of mercurials, but its exact mechanism, while also largely unconnected with changes