VANADATE ACTION ON RENAL PHOSPHATE-TRANSPORT

Insulin stimulates reabsorption of phosphate (Pi) in the renal proxima l tubule. Previous studies have shown that vanadate can mimic the acti on of insulin on various tissues. In the present study, we tested the action of vanadate on renal Pi transport both in control rats and in r ats made diabetic by injection of streptozotocin. Vanadate was adminis tered orally for 4 days by inclusion in drinking water (0.7 mg/ml). By the 4th day, vanadate treatment of control rats did not change acid-b ase status, plasma glucose or the filtered load of Pi, but the urinary excretion of Pi was reduced to 2.5 +/- 0.9 compared with 17.6 +/- 3.5 mu mol/mg creatinine (P < 0.02) in untreated control rats. However, N a+/Pi cotransport by isolated brush border membrane vesicles was not d ifferent between the two groups. Findings in parathyroidectomized rats were similar. By the 4th day of vanadate treatment of diabetic rats, there was reversal of polyuria, polydipsia and hyperglycemia with no c hange in acid base status. The filtered load of Pi was decreased by va nadate, and urinary Pi excretion also tended to decrease but not signi ficantly. The values for Pi excretion were 21.4 +/- 7.6 in vanadate tr eated diabetics and 36.1 +/- 4.5 mu mol/mg creatinine in untreated dia betics. In contrast to vanadate, daily injections of insulin did not c hange the filtered load of Pi but reduced urinary Pi excretion in diab etic rats to 15.6 +/- 2.2 mu mol/mg creatinine (P < 0.02). These findi ngs suggest that vanadate stimulated tubular Pi reabsorption in contro l rats but not in diabetic rats. Vanadate treatment of diabetic rats m ay tend to decrease tubular Pi reabsorption in contrast to the action of insulin.