Anesthetized dogs receiving an infusion of chlorothiazide and ethacrynic acid were given 600-ml infusions of distilled water or dilute dextrose solutions. The absolute rate of tubular sodium reabsorption was depressed, and the glomerular filtration rate was increased during the water loading, despite the associated decreases in plasma sodium concentration and decreases in the filtered load of sodium. The extent to which fractional sodium reabsorption decreased and the excretion of sodium increased was inversely related to the degree to which the filtered load of sodium was depressed as a result of the decreased plasma sodium concentration. We conclude that, in the presence of the diuretic blockade of distal tubular sodium reabsorption, infusion of water depresses proximal tubular reabsorption of sodium and that these changes are qualitatively similar to those previously observed during infusions of saline. Similar depression of tubular reabsorption of sodium and increased excretion of sodium occurred during water loading in the absence of diuretics in dogs undergoing saline diuresis, which presumably provided a high rate of distal sodium reabsorption before water loading. We suggest that volume expansion with water depresses proximal tubular reabsorption of sodium in a manner qualitatively similar to infusions of saline and that the extent to which sodium excretion is increased during water loading is dependent upon 1) the absolute extent to which proximal reabsorption is depressed, 2) the extent to which the filtered load of sodium is maintained in the presence of a falling concentration of sodium in plasma, and 3) the extent to which increased distal reabsorption compensates for the depressed proximal reabsorption of sodium. Mechanisms are suggested whereby the previously reported inverse relationship between plasma concentration of sodium and over-all tubular reabsorption of sodium may be only apparent, and could be the result of physiologic "glomerulotubular balance" during the specific experimental maneuvers.

Animals↗

PubMed1967

Demonstraton of a role of physical factors as determinants of the natriuretic response to volume expansion.

The importance of plasma protein concentration, renal vascular resistance, and arterial pressure as mediators of the natriuretic response to volume expansion was investigated in anesthetized dogs. Saline loading depressed plasma protein concentration and increased arterial pressure but did not decrease renal vascular resistance. Restoring plasma protein concentration by infusing hyperoncotic albumin increased sodium reabsorption and decreased sodium excretion during saline loading despite simultaneous decreases in renal vascular resistance and increases in arterial pressure. Infusion of "plasma" did not depress plasma protein concentration and produced natriuresis associated with increased arterial pressure and marked decreases in renal vascular resistance. Unilateral hemodynamic natriuresis was produced before "plasma" loading by the renal arterial infusion of acetylcholine, and the subsequent infusion of "plasma" resulted in much smaller increases in sodium excretion by the vasodilated kidney than by the control kidney. If perfusion pressure to both kidneys was then reduced by aortic constriction sodium excretion by the vasodilated kidney could be reduced to preloading (vasodilated) levels without reduced glomerular filtration, despite continued natriuresis in control kidneys which underwent vasodilatation in response to the infusion of plasma. Infusion of equilibrated whole blood did not alter plasma protein concentration or the hematocrit, and renal vascular resistance did not decrease. Sodium excretion was increased minimally or not at all by the infusion of blood despite increased arterial pressure and glomerular filtration. However, in kidneys vasodilated before infusing blood sodium excretion increased in response to the infusion in association with increased arterial pressure. This increased excretion of sodium by vasodilated kidneys during infusion of blood could be abolished by reducing perfusion pressure to the preloading level. These observations indicate that changes in plasma oncotic pressure, renal vascular resistance, and arterial pressure either alone or in combination are important variables determining the natriuretic response to volume expansion, and that the relative importance of each of these factors depends on the manner in which volume is expanded (viz., the infusion of saline, plasma, or blood).

Albumins↗

PubMed1967