The factors which influence sodium reabsorption in the nephron beyond the proximal tubule (distal tubule) remain unclear. Utilizing free water clearance (C,,,) as an index of distal-tubule sodium reabsorption, we have suggested that the development of a plateau in CHZ0 during hypotonic saline loading indicates that volume expansion limits the capacity of the distal nephron to reabsorb sodium (1). A maximal level of CIrz, was subsequently observed during hypertonic saline loading in man with diabetes insipidus (2). Other workers, however, have repeatedly been unable to demonstrate any limit in C,,, in the dog (3-5) and have suggested that saline loading does not alter the characteristics of sodium reabsorption in the distal nephron ( 5 ) . Moreover, a clear effect of volume expansion on the capacity of the loop of Henle to reabsorb sodium has not been demonstrated by microperfusion studies ( 6 ) .Previous clearance studies in the dog (7, 8 ) and recent micropuncture experiments in rats with congenital diabetes insipidus (9) have suggested that alterations in the passive back diffusion of water, even in the absence of antidiuretic hormone (ADH), may make the interpretation of CII,, as a measure of distal sodium reabsorption less useful. The present experiments were therefore performed in order to reevaluate whether a maximal level of CII,o is present in the dog and does reflect a limited capacity of the distal nephron to 73 7 reabsorb sodium, and to permit further insight into other factors which may influence distal sodium reabsorption. Studies were performed with sodium sulfate in order to dissociate sodium chloride supply to the distal nephron from distal tubular sodium supply, solute load, and urine flow rate.Methods. Experiments were performed on mongrel dogs weighing 20-29 kg. The preparation of the dogs was essentially as described in a previous report (1). Maximal hydration was achieved by the infusion of 2.5% glucose in water at 8-20 ml/min until urine osmolality was less than 100 mOsm/kg water.In 25 studies, 0.7-1.0% sodium sulfate was administered initially at a rate of 15 ml/min and subsequently increased to exceed urine flow rate by 10-15 ml/min. In 13 of the 25 studies, 0.3% sodium chloride was administered with 0.7% sodium sulfate. In 14 studies, a Blalock clamp was initially loosely positioned around one renal artery. During the sodium sulfate infusion, after control urine collections had been obtained from both kidneys, the clamp was tightened around the renal artery to produce an ipsilateral decrease in urine flow rate. Subsequently, the rate of the sodium sulfate infusion was increased as described above.Blood and urine were analyzed for osmolality, sodium, potassium, chloride, and inulin by standard methods (1).Results. The infusion of sodium sulfate
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