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The excretion of sodium by the kidney is influenced by changes in glomerular filtration rate (GFR), serum sodium concentration, adrenocortical activity, the quantity of nonreabsorbable solutes in the glomerular filtrate, and the volume of extracellular fluid (ECF) (1-4). Some of these factors alter sodium excretion by affecting the amount of sodium filtered; others modulate the tubular reabsorption of sodium. The mechanism whereby acute changes in the volume of ECF influence sodium excretion is not entirely clear. At least two factors, however, have been identified. Both the secretory rate of aldosterone and the GFR are influenced by alteration in the volume of ECF and may play important roles in the regulation of sodium excretion by volume. Alteration of sodium excretion by patients with Addison's disease in a parallel fashion with sodium intake and without detectable changes in GFR (5, 6) suggests that a third factor may be operative. Furthermore, a number of investigators (7-9) have shown that, under conditions where the volume of ECF was acutely altered in the face of fixed adrenocortical activity, sodium excretion varied independently of GFR, suggesting that changes in volume were in some manner influencing the tubular reabsorption of sodium independent of adrenocortical hormones.

the journal of clinical investigation/the journal of clinical investigation

Influence of Expansion of Extracellular Volume on Tubular Reabsorption of Sodium Independent of Changes in Glomerular Filtration Rate and Aldosterone Activity *