Inhibition of Renal Tubular Sodium Reabsorption by Hypernatremia.

In a recent study (1), we confirmed the observation of Bresler (2) and Toussaint and Vereerstraeten (3) that tubular sodium reabsorption (TNa) in dogs increases following plasma sodium (PNa) elevation. However, when the increase in filtered sodium (FNa) that usually accompanied an elevated PNa was eliminated by reducing glomerular filtration rate (GFR) with an aortic clamp, hypernatremia appeared to inhibit rather than stimulate TNa. Similar results have been obtained by Blythe and Welt (4), who found that sodium excretion during the infusion of hypertonic saline was above control when filtered sodium was reduced below control by inflating a balloon in the inferior vena cava. The micropuncture studies of Giebisch, Klose, and Windhager (5) in rats have also demonstrated that TNa is decreased by hypertonic saline infusions. In all these studies the depression of TNa was considered to be a consequence of hypernatremia per se. In each case, hypernatremia was induced by loading with hypertonic saline. The infusion of similar volumes of isotonic saline has been shown to inhibit TNa to a comparable degree (6-9). Therefore, the studies cited do not clearly differentiate between volume expansion and hypernatremia as the cause of the decreased TNa, nor, indeed, do they clearly establish that hyper-