Since the appearance in 1887 of von Schroeder's first publication (1) concerning the action of xanthine diuretics there has been much debate regarding the mechanism by which these substances produce diuresis. Similarly there has been considerable controversy as to the manner in which salyrgan and other organic mercury compounds increase the output of urine.
REVIEW OF LITERATUREIn the earlier work on xanthine diuresis investigators were chiefly interested in distinguishing between direct action on the renal cells and effects produced through changes in renal circulation. Von Schroeder (1) (2) concluded from his experiments that the effect of caffeine and related substances upon urine output was independent of circulatory changes. Loewi, Fletcher and Henderson (3) held the opposite point of view. They confirmed the observation, first made by Phillips and Bradford (4), that caffeine usually increases the volume of the kidney and considered this as evidence that diuresis was caused by dilatation of the renal blood vessels. Although this observation concerning kidney volume during caffeine diuresis is generally accepted, its significance has been questioned by Gottlieb and Magnus (5) because diuresis sometimes occurs without increase in kidney volume, by Brings and Molitor (6) who concluded that the increase in volume was of too short duration to be significant, and by Cushny (7) who pointed out that increase in kidney volume does not necessarily indicate vasodilatation.