The excretion of phosphate was studied in rats after release of complete unilateral ureteral obstruction of 24 hr duration. Marked differences were observed in the rate of excretion of phosphate between the control and the postreleased kidney. After release of unilateral ureteral obstruction, the fractional excretion of phosphate by the control kidney was greater than in normal rats, while the fractional excretion of phosphate by the experimental kidney was markedly decreased. The increased excretion of phosphate by the control kidney was abolished by prior parathyroidectomy and was attributed to an increase in the concentration of circulating parathyroid hormone. The low urinary excretion of phosphate by the experimental kidney could not be attributed to refractoriness of the renal tubule to the action of parathyroid hormone or to changes in the intrinsic capacity of the tubule to reabsorb phosphate. A marked decrease in the filtered load of phosphate is the most likely factor responsible for the low phosphate excretion by the experimental kidney. Support for this concept was obtained from studies in rats in which the filtered load of phosphate was decreased unilaterally by partially constricting the aorta proximal to the left renal artery. In these rats the fractional excretion of phosphate was considerably less in the constricted than in the contralateral normal kidney both before and after the administration of exogenous parathyroid hormone. In addition, a marked dissociation was observed between the rate of excretion of salt and water and the rate of excretion of phosphate in rats studied after release of unilateral ureteral ligation. Fractional excretion of sodium and water was greater in the experimental than in the control kidney whereas fractional excretion of phosphate was greater in the control than in the experimental kidney. These findings are consistent with the hypothesis that in the postobstructed kidney there is increased phosphate reabsorption in the proximal tubule and decreased sodium and water reabsorption in the distal tubule.