Abstract
Summary
Expansion of the extracellular fluid by saline infusion causes a decrease in net sodium reabsorption from the renal tubule and in net sodium absorption by the small intestine. The decreased net transport by the small intestine appears to be due to increased unidirectional flux of sodium from the extracellular fluid into the lumen, suggesting a similar mechanism in the renal tubule. Sodium-22 injected simultaneously with inulin into the renal artery appears in the urine before the inulin (“sodium precession”), demonstrating nonglomerular excretion of sodium via flux into the tubular lumen, and this method was used here to investigate this route of sodium excretion in dogs undergoing saline or water diuresis. A high degree of correlation was found between fractional excretion of 22Na+ in the precession peak and the rate of sodium excretion during saline loading. There was no correlation of fractional excretion of 22Na+ with urine flow rate during water diuresis. It is postulated that transtubular flux of sodium into the tubular lumen may contribute significantly to the renal Na excretion during salt loading.
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