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Research Article Free access | 10.1172/JCI105616
Thorndike Memorial Laboratory, Second and Fourth [Harvard] Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass.
†Recipient of U. S. Public Health Service Career Development Award 1-K3-AM-13,821-01.
Address requests for reprints to Dr. Laurence E. Earley, Thorndike Memorial Laboratory, Boston City Hospital, 818 Harrison Ave., Boston, Mass. 02118.
*Submitted for publication January 31, 1967; accepted April 11, 1967.
Aided in part by grants AM-5401-06 from the National Institutes of Health and NsG595 from the National Aeronautics and Space Administration.
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Thorndike Memorial Laboratory, Second and Fourth [Harvard] Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass.
†Recipient of U. S. Public Health Service Career Development Award 1-K3-AM-13,821-01.
Address requests for reprints to Dr. Laurence E. Earley, Thorndike Memorial Laboratory, Boston City Hospital, 818 Harrison Ave., Boston, Mass. 02118.
*Submitted for publication January 31, 1967; accepted April 11, 1967.
Aided in part by grants AM-5401-06 from the National Institutes of Health and NsG595 from the National Aeronautics and Space Administration.
Find articles by Earley, L. in: JCI | PubMed | Google Scholar
Published July 1, 1967 - More info
Anesthetized dogs receiving an infusion of chlorothiazide and ethacrynic acid were given 600-ml infusions of distilled water or dilute dextrose solutions. The absolute rate of tubular sodium reabsorption was depressed, and the glomerular filtration rate was increased during the water loading, despite the associated decreases in plasma sodium concentration and decreases in the filtered load of sodium. The extent to which fractional sodium reabsorption decreased and the excretion of sodium increased was inversely related to the degree to which the filtered load of sodium was depressed as a result of the decreased plasma sodium concentration. We conclude that, in the presence of the diuretic blockade of distal tubular sodium reabsorption, infusion of water depresses proximal tubular reabsorption of sodium and that these changes are qualitatively similar to those previously observed during infusions of saline. Similar depression of tubular reabsorption of sodium and increased excretion of sodium occurred during water loading in the absence of diuretics in dogs undergoing saline diuresis, which presumably provided a high rate of distal sodium reabsorption before water loading.
We suggest that volume expansion with water depresses proximal tubular reabsorption of sodium in a manner qualitatively similar to infusions of saline and that the extent to which sodium excretion is increased during water loading is dependent upon 1) the absolute extent to which proximal reabsorption is depressed, 2) the extent to which the filtered load of sodium is maintained in the presence of a falling concentration of sodium in plasma, and 3) the extent to which increased distal reabsorption compensates for the depressed proximal reabsorption of sodium. Mechanisms are suggested whereby the previously reported inverse relationship between plasma concentration of sodium and over-all tubular reabsorption of sodium may be only apparent, and could be the result of physiologic “glomerulotubular balance” during the specific experimental maneuvers.