Advertisement
Research Article Free access | 10.1172/JCI105540
Renal-Electrolyte Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pa.
†Work supported by a Research Career Development Award from the National Institute of Arthritis and Metabolic Diseases, U. S. Public Health Service grant 5K3AM18582-04,-05. Address requests for reprints to Dr. Martin Goldberg, 860 Gates Pavilion, 3400 Spruce Street, Philadelphia, Pa. 19104.
‡Visiting investigator, University of Pennsylvania School of Medicine. Present address: Second Dept. of Medicine, Poznan, Poland.
§Present address: British-American Hospital, Lima, Peru.
*Submitted for publication August 11, 1966; accepted November 14, 1966.
Supported by U. S. Public Health Service grants HE 00340-C16-C17 and HE 07284-04-05.
A preliminary report of this work was presented at the 50th Annual Meeting of the Federation of American Societies for Experimental Biology in Atlantic City, N. J., April 12, 1966. Published in Fed. Proc. 1966, 25, 203.
Find articles by Goldberg, M. in: JCI | PubMed | Google Scholar
Renal-Electrolyte Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pa.
†Work supported by a Research Career Development Award from the National Institute of Arthritis and Metabolic Diseases, U. S. Public Health Service grant 5K3AM18582-04,-05. Address requests for reprints to Dr. Martin Goldberg, 860 Gates Pavilion, 3400 Spruce Street, Philadelphia, Pa. 19104.
‡Visiting investigator, University of Pennsylvania School of Medicine. Present address: Second Dept. of Medicine, Poznan, Poland.
§Present address: British-American Hospital, Lima, Peru.
*Submitted for publication August 11, 1966; accepted November 14, 1966.
Supported by U. S. Public Health Service grants HE 00340-C16-C17 and HE 07284-04-05.
A preliminary report of this work was presented at the 50th Annual Meeting of the Federation of American Societies for Experimental Biology in Atlantic City, N. J., April 12, 1966. Published in Fed. Proc. 1966, 25, 203.
Find articles by Wojtczak, A. in: JCI | PubMed | Google Scholar
Renal-Electrolyte Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pa.
†Work supported by a Research Career Development Award from the National Institute of Arthritis and Metabolic Diseases, U. S. Public Health Service grant 5K3AM18582-04,-05. Address requests for reprints to Dr. Martin Goldberg, 860 Gates Pavilion, 3400 Spruce Street, Philadelphia, Pa. 19104.
‡Visiting investigator, University of Pennsylvania School of Medicine. Present address: Second Dept. of Medicine, Poznan, Poland.
§Present address: British-American Hospital, Lima, Peru.
*Submitted for publication August 11, 1966; accepted November 14, 1966.
Supported by U. S. Public Health Service grants HE 00340-C16-C17 and HE 07284-04-05.
A preliminary report of this work was presented at the 50th Annual Meeting of the Federation of American Societies for Experimental Biology in Atlantic City, N. J., April 12, 1966. Published in Fed. Proc. 1966, 25, 203.
Find articles by Ramirez, M. in: JCI | PubMed | Google Scholar
Published March 1, 1967 - More info
To study the renal medullary transport and accumulation of urea in dogs independent of water transport, we obliterated the medullary electrolyte gradient by a sustained ethacrynic acid diuresis. Infusions of urea were also given at various rates to vary urinary urea concentration. In the steady state, the kidneys were removed, and slices were analyzed for water, urea, and electrolytes. In every experiment in 15 dogs over a range of urinary urea concentration from 19 to 230 mmoles per L and urine flow from 0.5 to 9.7 ml per minute per kidney, an intrarenal urea gradient persisted, and urinary urea concentration was always lower than papillary water urea concentration. The magnitude of this uphill urinary-papillary gradient (mean ± SE = - 21 ± 2.9 mmoles per L) was not affected by hemorrhagic hypotension or a nonprotein diet.
In 12 additional experiments begun similarly, inhibitors were infused into one renal artery. Both iodoacetate, an inhibitor of anaerobic glycolysis, and acetamide, an analogue of urea, markedly and significantly reduced both the intrarenal urea gradient and the uphill urinary-papillary gradient. In contrast, cyanide, an inhibitor of oxidative metabolism, had no observable effect on the urea gradients. The data are best explained by postulating an active transport system for urea in the medullary collecting duct deriving its energy from anaerobic glycolysis.