The effect of glucose on urinary cation excretion during chronic extracellular volume expansion in normal man.

Both glucose administration and extracellular volume expansion augment urinary calcium and magnesium excretion. While volume expansion also augments sodium excretion, glucose induces an antinatriuresis. To examine the interrelationships of volume expansion and of glucose administration on sodium, calcium, and magnesium excretion, the effects of glucose were evaluated during clearance studies in the same subjects before and after chronic extracellular volume expansion produced by desoxycorticosterone acetate (DOCA) and a normal dietary sodium intake. The augmentation of U(Ca)V and U(Mg)V by glucose was simply additive to the increments in divalent cation excretion caused by "escape" from the sodium-retaining effects of DOCA. Glucose administration reduced U(Na)V, an effect exaggerated after DOCA escape and associated with reductions in volume/glomerular filtration rate (V/GFR) and C(Na) + C(H2O)/GFR, suggesting augmented proximal tubular reabsorption. Before glucose, U(Na) was inversely correlated with U(G), and after glucose administration C(Na)/GFR was inversely correlated with T(G)/GFR. We propose that the availability of glucose in the proximal tubule stimulates Na reabsorption while delaying development of a chloride diffusion potential, thereby inhibiting tubular reabsorption of Ca and Mg.