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Previous studies have indicated that acute reductions in glomerular filtration rate (GFR), during loading with nonreabsorbable solute, increase the fraction of the filtered sodium load reabsorbed (1-3). The renal tubular sites at which this enhanced reabsorption develops have not been elucidated. Recent studies from this laboratory in which mannitol loads were administered to salt-depleted subjects with modest reductions in GFR suggested that sodium reabsorption was enhanced within the proximal tubule (4). However, it was not possible to determine whether renal hemodynamics or other, perhaps hormonal, factors were responsible for the increased reabsorption at this site. The present studies were designed to evaluate the specific effects of a reduction in GFR produced by renal arterial constriction on tubular sodium reabsorption. We propose that renal arterial constriction during loading with nonreabsorbable solute provokes an enhanced reabsorption of sodium, in large part within the proximal tubule.

Effects of unilateral renal arterial constriction on tubular reabsorption of sodium and water during an osmotic diuresis.