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Research Article Free access | 10.1172/JCI105611
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Donald W. Seldin, Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5223 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication September 13, 1966; accepted March 22, 1967.
Supported in part by grants 5-SOI FR-5426-05 and 5-TI HE-5469 from the National Institutes of Health and in part by a grant from the Dallas Heart Association.
Find articles by Eknoyan, G. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Donald W. Seldin, Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5223 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication September 13, 1966; accepted March 22, 1967.
Supported in part by grants 5-SOI FR-5426-05 and 5-TI HE-5469 from the National Institutes of Health and in part by a grant from the Dallas Heart Association.
Find articles by Suki, W. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Donald W. Seldin, Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5223 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication September 13, 1966; accepted March 22, 1967.
Supported in part by grants 5-SOI FR-5426-05 and 5-TI HE-5469 from the National Institutes of Health and in part by a grant from the Dallas Heart Association.
Find articles by Rector, F. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. Donald W. Seldin, Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5223 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication September 13, 1966; accepted March 22, 1967.
Supported in part by grants 5-SOI FR-5426-05 and 5-TI HE-5469 from the National Institutes of Health and in part by a grant from the Dallas Heart Association.
Find articles by Seldin, D. in: JCI | PubMed | Google Scholar
Published July 1, 1967 - More info
The functional characteristics of the ascending limb of Henle's loop were examined during hypotonic saline infusion by measuring solutefree water clearance (CH2O) at varying rates of solute delivery. The influence of expansion of extracellular volume was studied by comparing CH2O during hypotonic saline diuresis in normal dogs with dogs whose extracellular volume had been expanded acutely by saline infusions or chronically by the administration of deoxycorticosterone acetate and salt.
In normal animals hypotonic saline infusions greatly increased urine flow (V) and CH2O without appreciably augmenting osmolar clearance (Cosm). CH2O was, therefore, analyzed as a function of V, rather than Cosm, since V was the best estimate of delivery of filtrate to the diluting segment. CH2O increased as a linear function of V without any evidence of saturation.
The validity of interpreting increases in CH2O and V as indications of increased sodium reabsorption and delivery was reinforced by tissue studies that disclosed a rise in papillary osmolality with rising urine flows. The observed increase in CH2O and V could not, therefore, be due to a decrease in back diffusion of solute-free water as a result of a diminished osmotic driving force, but probably represented increased formation consequent to augmented delivery as a result of decreased fractional reabsorption in the proximal tubule.
In animals whose extracellular volume was acutely or chronically overexpanded before the infusion of hypotonic saline, sodium excretion was greater, and CH2O less, at any given V. Although the curve relating CH2O to V was flatter than in the control group, no tubular maximum was observed. The diminished CH2O in this group was interpreted to mean that massive expansion of extracellular volume inhibits sodium reabsorption in the ascending limb of Henle's loop.
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