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Research Article Free access | 10.1172/JCI106118

The relationship between peritubular capillary protein concentration and fluid reabsorption by the renal proximal tubule

Barry M. Brenner, Kenneth H. Falchuk, Robert I. Keimowitz, and Robert W. Berliner

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland 20014

Find articles by Brenner, B. in: PubMed | Google Scholar

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland 20014

Find articles by Falchuk, K. in: PubMed | Google Scholar

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland 20014

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

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland 20014

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

Published August 1, 1969 - More info

Published in Volume 48, Issue 8 on August 1, 1969
J Clin Invest. 1969;48(8):1519–1531. https://doi.org/10.1172/JCI106118.
© 1969 The American Society for Clinical Investigation
Published August 1, 1969 - Version history
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Abstract

The relationship between peritubular capillary protein concentration and rate of sodium reabsorption by the rat proximal tubule was examined using free-flow recollection micropuncture techniques. Tubule fluid-to-plasma inulin ratios were measured before, during, and at successive intervals after brief (15-25 sec) intra-aortic injections (at the level of the renal artery) of colloid-free, isoncotic, and hyperoncotic solutions. Arterial hematocrit and protein concentrations were measured simultaneously in these rats. In other rats, total protein concentration of peritubular capillary blood plasma was determined before, during, and after these same infusions with a newly described submicroliter fiber-optic colorimeter.

In the 15-25 sec interval necessary to infuse 2 ml of these test solutions, fractional and absolute sodium reabsorption varied directly with peritubular capillary colloid osmotic pressure, declining during infusion of colloid-free solutions, increasing during hyperoncotic infusions, and remaining unchanged during isoncotic infusions.

In the subsequent 20-min interval after intra-aortic injection of these test solutions, capillary protein concentration remained at (isoncotic infusions) or returned to (colloid-free and hyperoncotic fluids) control values. Whereas reabsorption after colloid-free solutions returned to base line levels in parallel with the return in capillary protein concentration, after colloid infusions (which resulted in continued expansion of extracellular fluid volume), a progressive decline in reabsorption was observed.

These results afford strong evidence that peritubular capillary colloid osmotic pressure is one important determinant of proximal sodium reabsorption. Nevertheless it is apparent that mechanisms other than or in addition to this must be invoked to explain the delayed inhibition of reabsorption that accompanies expansion of extracellular fluid volume by colloid solutions.

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