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Research Article Free access | 10.1172/JCI106067

Failure to demonstrate a hormonal inhibitor of proximal sodium reabsorption

Fred S. Wright, Barry M. Brenner, Cleaves M. Bennett, Robert I. Keimowitz, Robert W. Berliner, Robert W. Schrier, Pierre J. Verroust, Hugh E. De Wardener, and Heinz Holzgreve

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

Find articles by Wright, F. in: JCI | PubMed | Google Scholar

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

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

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

Find articles by Bennett, C. in: JCI | PubMed | Google Scholar

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

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

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

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

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

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

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

Find articles by Verroust, P. in: JCI | PubMed | Google Scholar

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

Find articles by De Wardener, H. in: JCI | PubMed | Google Scholar

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

Department of Medicine, Charing Cross Hospital Medical School, London, England

Department of Internal Medicine II, University of Cologne, Köln-Merheim, Germany

Find articles by Holzgreve, H. in: JCI | PubMed | Google Scholar

Published June 1, 1969 - More info

Published in Volume 48, Issue 6 on June 1, 1969
J Clin Invest. 1969;48(6):1107–1113. https://doi.org/10.1172/JCI106067.
© 1969 The American Society for Clinical Investigation
Published June 1, 1969 - Version history
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Abstract

Recently, it has been reported that a humoral inhibitor of proximal sodium reabsorption could be detected in plasma, and dialysates of plasma, of rats and dogs undergoing saline diuresis. We have repeated these studies using similar techniques and protocols. Fractional sodium reabsorption by the proximal tubule (as estimated in free-flow micropuncture studies from tubule fluid-to-plasma inulin ratios) was found not to be lower during infusion of “natriuretic” plasma than during subsequent infusion of “hydropenic” plasma. Similarly, infusion of natriuretic plasma failed to prolong reabsorptive half-time of the shrinking drop beyond that seen during hydropenic plasma infusion. No increase in urine volume or rate of sodium excretion was observed during the period of natriuretic plasma infusion, nor did natriuretic plasma result in an increase in these measures in rats undergoing water diuresis.

It also has been reported that dialysates of natriuretic plasma, but not of hydropenic plasma, when placed directly into the tubule lumen, inhibit proximal sodium reabsorption. In double blind studies carried out independently in Bethesda, London, and Cologne, we failed to detect the presence of a dialyzable inhibitor in natriuretic plasma. Finally, in contrast to other recent reports, we were unable to detect inhibitory activity in plasma obtained from dogs during the “escape” phase of chronic deoxycorticosterone acetate administration.

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