Increment In Sodium Excretion Research Articles

Effects of hypotonic saline loading in hydrated dog: evidence for a saline-induced limit on distal tubular sodium transport.

We performed studies on dogs under hydrated conditions, utilizing the rate of free water formation (C(H2O)) as an index of the rate of distal tubular sodium transport. Since C(H2O) could be progressively increased with no evidence of a maximal rate during loading with hypotonic (2.5%) mannitol, it was concluded that there is no limit on distal tubular sodium transport during mannitol loading. In contrast, during hypotonic (0.45%) saline loading C(H2O) rose initially, but as urine flow (V) exceeded 25% of the filtered load C(H2O) attained maximal levels (up to 20% of the filtered load) and remained stable as V increased to 50% of the filtered load. It was concluded that saline loading progressively inhibits proximal sodium reabsorption. Initially, the distal tubule absorbes a large fraction of the proximal rejectate and sodium excretion rises slightly. Eventually, an alteration in distal sodium transport appears which culminates in a maximal rate or transport limit. This distal transport limit provoked by saline loading could not be characterized by a classical Tm as seen with glucose and does not seem to be consequent to high rates of flow through the distal tubule. Regardless of the precise nature of this limit, the major increment in sodium excretion develops during saline loading only after saline alters the capacity of the distal tubule to transport sodium.

Mathematical aspects of renal function: The dependence of solute reabsorption on water reabsorption, and the mechanism of osmotic natriuresis

The effect of changes in water reabsorption upon solute reabsorption in the renal tubule has been examined theoretically by writing kinetic equations for solute and water reabsorption at any point in a uniform segment and integrating over the length of the segment. In an isosmotic segment, a linear or nearly linear relationship between reabsorbed sodium, z 0− z, and the quantity m 1n z/ z 0, where m is the filtered load of unreabsorbable solute, should be seen during infusion of isosmotic mannitol (or similar solute), whether sodium reabsorption follows first-order, pump, or pump-and-leak kinetics. However, the increment in sodium excretion which has been observed experimentally following such infusions is seen in mathematical models only if there is a substantial leak, and is therefore attributable to increased passive influx of sodium rather than reduced active efflux. The excretion of other reabsorbable solutes also increases with outflow, unless their reabsorption is independent of concentration. For at least half-saturated pumps, a roughly linear increase in solute excretion occurs when flow increases. The intercept of this line can (in theory) provide an estimate of the T m and Michaelis constant, even at constant plasma concentration and filtration rate. Outflow concentration may fail to vary appreciably with flow under some conditions, even though reabsorption is concentration dependent.