1. In order to study the relationship between sodium and glucose transport along the nephron, clearance and micropuncture experiments were performed in 16 dogs before and after administration of diuretics with different sites of action.

2. Administration of acetazolamide, 20 mg (90 μmol)/kg, in nine dogs significantly reduced proximal tubular reabsorption of sodium and glucose and slightly increased ‘distal’ delivery of glucose. Since no glycosuria developed despite significant natriuresis, the increased ‘distal’ load of glucose must have been reabsorbed.

3. The possible site of this ‘distal’ glucose reabsorption was further studied in seven dogs which had received extracellular volume expansion to 10% of body weight and acetazolamide, 10 mg (45 μmol)/kg, to suppress proximal tubule reabsorption. When frusemide, 10 mg (30 μmol)/kg, was added, fractional glucose excretion increased from 0·3 to 2% in the absence of additional proximal tubular effect. However, the frusemide effect on ‘distal’ glucose transport was far smaller than that on sodium since fractional sodium excretion reached 40%.

4. Our results indicate a good correlation between sodium and glucose transport in the proximal tubule since both are inhibited by acetazolamide. Administration of large doses of frusemide leads to a modest glycosuria, probably by inhibition of glucose reabsorption in the loop of Henle. However, frusemide effect on the proximal tubule of deep nephrons cannot be completely excluded. The large discrepancy in the magnitude of natriuresis and glycosuria suggests dissociation of ‘distal’ sodium and glucose transport. Alternative explanations for the frusemide-induced glycosuria are also discussed.

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