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Although the excretion of ammonia into urine has been extensively studied, there is little information in animals or man concerning the quantitative and regulatory aspects of the ammonia released into the renal veins. Previous observations in this laboratory and in others have demonstrated that the kidney consistently releases ammonia into the systemic circulation of normal subjects and patients with liver disease whose arterial ammonia concentrations are normal (1-5). Patients with liver disease and moderate to marked hyperammonemia, however, usually release minimal quantities of ammonia into their renal veins and occasionally exhibit renal uptake of ammonia from the circulation (2). -In order to further define the possible role of the blood ammonia concentration on renal ammonia release, acute hyperammonemia has been induced in normal subjects and the subsequent changes in renal vein ammonia release and urine ammonia excretion determined. METHODSNine patients without hepatic or renal disease were studied. All were hospitalized ambulatory males ranging in age from 28 to 49 years. Subj ects were studied in the recumbent position after an overnight fast. In order to initiate a water diuresis, 1,000 to 1,500 ml of water was ingested 30 minutes to 1 hour before each procedure. A constant intravenous infusion (Bowman pump) which delivered 14 to 18 mg of para-aminohippurate (PAH) per minute was maintained throughout the study period and was preceded by a priming dose calculated to provide plasma levels of approximately 2 mg per 100 ml. The water diuresis was maintained throughout the procedure by the intravenous infusion of 5 per cent dextrose and water at a rate of 15 to 20 ml per minute. Arterial samples were obtained from a brachial artery and renal venous samples from the * This investigation was supported (in part) by a research grant (Public Health Service A-3255) from the National Institutes of Health, Bethesda, Md. tThis paper was presented (in part) at the Southern Society for Clinical Research, New Orleans, La., January 23, 1960. right renal vein by way of a no. 8 catheter. Control voided urine specimens were collected during and after equilibration of the PAH infusion. Baseline arterial and renal venous samples were begun 45 to 60 minutes after the PAH infusion was started. Each patient received an intravenous infusion of 0.155 M ammonium lactate at a rate of 0.50 mEq of ammonia per minute for 30 minutes and 0.75 mEq of ammonia per minute for the subsequent 15 minutes. Serial arterial-renal venous ammonia differences were obtained at 15-minute intervals during the infusion and at the 15 minute post-infusion period. Voided urine samples collected in an oil-toluene mixture were obtained at 15-to 30-minute intervals during the infusion and in 4 subjects for 30 to 60 minutes after the infusion was terminated.Blood and urine ammonia was measured by a modification (6) of the microdiffusion method of Brown, Duda, Korkes and Handler (7). PAH concentration in blood and infusion media was determined by the method...

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