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Research Article Free access | 10.1172/JCI105614

Effects of Hypotonic Saline Loading in Hydrated Dog: Evidence for a Saline-induced Limit on Distal Tubular Sodium Transport

Richard M. Stein, Ruth G. Abramson, Thomas Kahn, and Marvin F. Levitt

Section of Renal Diseases, Department of Medicine, The Mount Sinai School of Medicine, New York, N. Y.

Renal Unit, Medical Service, U. S. Public Health Service Hospital, Staten Island, N. Y.

†

Address requests for reprints to Dr. Richard M. Stein, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.

‡

National Institutes of Health postdoctoral fellow.

*

Submitted for publication December 7, 1966; accepted April 11, 1967.

These studies were supported by U. S. Public Health Service research grant HE-08535 from the National Heart Institute, and CCIC grant P-67-22 from the Bureau of Health Services, Division of Direct Health Services, U. S. Public Health Service.

Presented in abstract from at the Fifty-Seventh Annual Meeting of the American Society for Clinical Investigation, May, 1965 (J. clin. Invest. 1965, 44, 1100).

Find articles by Stein, R. in: JCI | PubMed | Google Scholar

Section of Renal Diseases, Department of Medicine, The Mount Sinai School of Medicine, New York, N. Y.

Renal Unit, Medical Service, U. S. Public Health Service Hospital, Staten Island, N. Y.

†

Address requests for reprints to Dr. Richard M. Stein, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.

‡

National Institutes of Health postdoctoral fellow.

*

Submitted for publication December 7, 1966; accepted April 11, 1967.

These studies were supported by U. S. Public Health Service research grant HE-08535 from the National Heart Institute, and CCIC grant P-67-22 from the Bureau of Health Services, Division of Direct Health Services, U. S. Public Health Service.

Presented in abstract from at the Fifty-Seventh Annual Meeting of the American Society for Clinical Investigation, May, 1965 (J. clin. Invest. 1965, 44, 1100).

Find articles by Abramson, R. in: JCI | PubMed | Google Scholar

Section of Renal Diseases, Department of Medicine, The Mount Sinai School of Medicine, New York, N. Y.

Renal Unit, Medical Service, U. S. Public Health Service Hospital, Staten Island, N. Y.

†

Address requests for reprints to Dr. Richard M. Stein, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.

‡

National Institutes of Health postdoctoral fellow.

*

Submitted for publication December 7, 1966; accepted April 11, 1967.

These studies were supported by U. S. Public Health Service research grant HE-08535 from the National Heart Institute, and CCIC grant P-67-22 from the Bureau of Health Services, Division of Direct Health Services, U. S. Public Health Service.

Presented in abstract from at the Fifty-Seventh Annual Meeting of the American Society for Clinical Investigation, May, 1965 (J. clin. Invest. 1965, 44, 1100).

Find articles by Kahn, T. in: JCI | PubMed | Google Scholar

Section of Renal Diseases, Department of Medicine, The Mount Sinai School of Medicine, New York, N. Y.

Renal Unit, Medical Service, U. S. Public Health Service Hospital, Staten Island, N. Y.

†

Address requests for reprints to Dr. Richard M. Stein, U. S. Public Health Service Hospital, Staten Island, N. Y. 10304.

‡

National Institutes of Health postdoctoral fellow.

*

Submitted for publication December 7, 1966; accepted April 11, 1967.

These studies were supported by U. S. Public Health Service research grant HE-08535 from the National Heart Institute, and CCIC grant P-67-22 from the Bureau of Health Services, Division of Direct Health Services, U. S. Public Health Service.

Presented in abstract from at the Fifty-Seventh Annual Meeting of the American Society for Clinical Investigation, May, 1965 (J. clin. Invest. 1965, 44, 1100).

Find articles by Levitt, M. in: JCI | PubMed | Google Scholar

Published July 1, 1967 - More info

Published in Volume 46, Issue 7 on July 1, 1967
J Clin Invest. 1967;46(7):1205–1214. https://doi.org/10.1172/JCI105614.
© 1967 The American Society for Clinical Investigation
Published July 1, 1967 - Version history
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Abstract

We performed studies on dogs under hydrated conditions, utilizing the rate of free water formation (CH2O) as an index of the rate of distal tubular sodium transport. Since CH2O could be progressively increased with no evidence of a maximal rate during loading with hypotonic (2.5%) mannitol, it was concluded that there is no limit on distal tubular sodium transport during mannitol loading. In contrast, during hypotonic (0.45%) saline loading CH2O rose initially, but as urine flow (V) exceeded 25% of the filtered load CH2O attained maximal levels (up to 20% of the filtered load) and remained stable as V increased to 50% of the filtered load. It was concluded that saline loading progressively inhibits proximal sodium reabsorption. Initially, the distal tubule absorbes a large fraction of the proximal rejectate and sodium excretion rises slightly. Eventually, an alteration in distal sodium transport appears which culminates in a maximal rate or transport limit. This distal transport limit provoked by saline loading could not be characterized by a classical Tm as seen with glucose and does not seem to be consequent to high rates of flow through the distal tubule. Regardless of the precise nature of this limit, the major increment in sodium excretion develops during saline loading only after saline alters the capacity of the distal tubule to transport sodium.

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