Evidence for a Direct Effect of Serum Sodium Concentration on Sodium

The mechanisms that modulate the renal excretion of sodium have not been completely defined. Impressive evidence has been assembled establishing the individual contributions of alterations in glomerular filtration rate (GFR), adrenal cortical activity, and some function of effective extracellular fluid (ECF) volume (1-4). A fourth factor influencing sodium excretion is the restraining action of unreabsorbed non-ionic solutes, such as mannitol, and of unreabsorbed anions, such as sulfate. Finally, it has been suggested that the concentration of serum sodium might also influence sodium excretion. The role of the concentration of serum sodium per se in the regulation of sodium reabsorption, however, is not nearly so well defined. This uncertainty stems largely from the fact that manipulations designed to alter the concentration of serum sodium usually change the filtered load of soduim, ECF volume, and perhaps adrenocortical activity, in such a manner that the contribution of serum sodium is obscured. In the case of hypernatremiiia, Baldwin, Kahana and Clarke (5) showed that the natriuresis induced by the administration of hypertonic saline correlated more closely with the elevated serum sodium concentration than with the increased filtered load of sodium and attributed this to a direct suppression of renal tubular sodium reabsorption. Selkurt and Post (6), however, found that during the infusion of hypertonic saline into one renal artery of the dog, tubular sodium reabsorption remained constant or increased, and that the natriuresis on