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Research Article Free access | 10.1172/JCI105551

Ammonia Movement in the Small Intestine: Preferential Transport by the Ileum

Sanford M. Mossberg and George Ross

Department of Gastroenterology, Medical Division and Laboratory Division, Montefiore Hospital and Medical Center, New York. N. Y.

†

Address requests for reprints to Dr. Sanford M. Mossberg, 33 Quaker Ridge Rd., New Rochelle, N. Y.

*

Submitted for publication May 4, 1966; accepted December 8, 1966.

Supported by U. S. Public Health Service grant AM-07905 from the National Institute of Arthritis and Metabolic Diseases.

Find articles by Mossberg, S. in: JCI | PubMed | Google Scholar

Department of Gastroenterology, Medical Division and Laboratory Division, Montefiore Hospital and Medical Center, New York. N. Y.

†

Address requests for reprints to Dr. Sanford M. Mossberg, 33 Quaker Ridge Rd., New Rochelle, N. Y.

*

Submitted for publication May 4, 1966; accepted December 8, 1966.

Supported by U. S. Public Health Service grant AM-07905 from the National Institute of Arthritis and Metabolic Diseases.

Find articles by Ross, G. in: JCI | PubMed | Google Scholar

Published April 1, 1967 - More info

Published in Volume 46, Issue 4 on April 1, 1967
J Clin Invest. 1967;46(4):490–498. https://doi.org/10.1172/JCI105551.
© 1967 The American Society for Clinical Investigation
Published April 1, 1967 - Version history
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Abstract

Isolated, surviving sacs of everted small intestine were used to characterize ammonia transport in the golden hamster. Jejunal and ileal sacs incubated aerobically in ammonia-free test solution liberated the same quantity of ammonia as did sacs that were filled and immediately emptied of their contents, indicating no significant evolution of metabolic ammonia.

Under aerobic conditions, ileal sacs transferred a solution of high ammonia content from the mucosal surface to the serosal surface against a concentration gradient. This transport was not glucose dependent and exhibited first-order Michaelis-Menten kinetics. Inhibition of absorption occurred with anaerobiosis, 2,4-dinitrophenol, and sodium cyanide. In jejunal segments ammonia was not transported against an adverse chemical gradient. Ileal ammonia absorption was accompanied by bicarbonate secretion and acidification of the serosal solution. Both bicarbonate movement and pH gradients were abolished by inhibitors of ammonia transport. In the jejunum, the absence of ammonia movement occurred in association with minimal bicarbonate secretion and no appreciable change in serosal pH.

Despite the creation of hydrogen ion gradients tending to augment or to retard ammonia absorption by nonionic diffusion, ammonia movement was unaffected, i.e., relative acidification of serosal contents did not augment ammonia absorption, and relative alkalinization of serosal fluid caused no inhibition of ammonia transport. In the absence of bicarbonate ion, ammonia transport did not occur. The significance of these findings is discussed with consideration of both ionic and nonionic mechanisms of ammonia movement. It is suggested that ammonia is absorbed in the ileum by active ionic transport.

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