Mobilization of ascites was studied in 20 anesthetized dogs with experimental cirrhosis following a mannitol- or furosemide-induced diuresis. Observations were made at 2 h following the drug, at which time the diuresis was invariably completed, and repeated at 4 h following a 2-h recovery period, during which the ureters were clamped to prevent further urinary losses. In the furosemide group the mean urinary loss was 459 +/- 6 ml and was accompanied by a decline in central venous pressure and hemoconcentration. At 2 h plasma volume had declined by 14% from control values, but at 4 h plasma replenishment was 99% complete. At this time ascites volume had decreased by 467 ml, acting as the major source for vascular replenishment. In the mannitol group, the average urinary loss was 190 +/- 10 ml and was accompanied by maintenance of venous pressure, lack of hemoconcentration, and hyponatremia. At 2 h plasma volume had expanded from control values by 22%, but at 4 h vascular replenishment was only 78% complete. The average ascites volume had decreased by only 55% of the diuretic loss, and was mobilized by a complex sequence of events involving movement of intracellular water.