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Continuous perfusion of the dog's renal artery at pressures averaging 200 mm Hg resulted in natriuresis, increased osmolar clearance, and increase in urine volume. The diuresis was typified by a decrease in TcHH2O, and in some instances positive free water clearance resulted. U/P of osmolality also declined, in some cases below unity. The above changes were observed in the absence of increase in glomerular filtration rate, as measured by creatinine clearance. The reductions in TcHH2O and U/P osmolality were correlated with decrease in the papillary to cortical sodium gradient. Thus, a washout of the osmotic gradient appeared to be the mechanism responsible for the decrease in ability of ADH to concentrate the urine. Because sodium and total osmolar load did not increase during the elevated pressure perfusion, decreased tubular reabsorption must have accounted for the natriuresis and enhanced osmolar clearance. It is speculated that the papillary sodium washout might indirectly influence sodium reabsorption by the ascending limb of the loop of Henle. The possibility is also considered that a mechanism of intrarenal hormonal regulation, responsive to changes in arterial pressure, might be responsible for the increased sodium clearance.