Sodium Excretion by the Mammalian Kidney

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Abstract
Na excretion by the mammalian kidney during varied physiological circumstances is regulated by changes in glomerular filtration rate (GFR) or by alteration in tubular reabsorption. Frequently it is difficult to decide which is the dominant mechanism. Often when alterations in filtration rate are undetectable or small, investigators conclude that tubular reactivity toward Na has been altered. In the opinion of the reviewer, the possibility remains open that small alterations in GFR undetectable by present techniques, may account for changes in UNaV often considered significant in certain experiments of an acute nature. As a corollary, it seems unwarranted to conclude that whenever an alteration in uNav occurs in the absence of detectable changes in GFR, a change in endocrine regulation (pituitary, adrenal) is the necessary alternative. Much more work is needed to characterize the Na transfer system. Perhaps a cation exchange system, such as proposed by Binkley is involved. The studies of Ussing, Linderhol and Huf concerned with the active transport of Na and other ions across the frog''s skin in relation to potential differences may have an interesting connotation concerning the possibility that a similar Na pump may be concerned with active transport of Na ions by the kidney tubules. Understanding of the mechanism of intestinal absorption of ions (e.g. Cl) against concentration gradients may supply clues. An enzyme-like mechanism has been described in the cat erythrocyte membrane which reduces the activation energy necessary for Na penetration, a mechanism from which K is partially or completely excluded. Ultimately, when more is known about the characteristics of the enzyme systems which supply energy for the transfer system, a better foundation will be supplied for understanding how influence is exerted on the reabsorptive systems by hormones, such as the adrenal steroids, and by the other regulatory influences.

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