Effects of physiologic hyperinsulinemia on renal phosphate handling in the rat: a role for calcium

: In a recent study in acutely parathyroidectomized, fasted rats, infused with parathyroid hormone (PTH), superimposition of euglycemic hyperinsulinemia within the physiologic range completely reversed the decline in tubular reabsorption of Pi (TRPi) induced by PTH. As an extension of these observations on insulin as a counterregulator of Pi homeostatis, the present results demonstrated that similar insulin administration prevented a decrease in TRPi when PTH infusion was superimposed. This was, moreover, observed in the fed state and at doses of insulin which did not stimulate renal cortical Na-K-ATPase activity. Subsequent studies addressed the role of insulin in a PTH-independent phosphaturic state, namely that induced by Pi loading. Under such conditions and while the resultant hypocalcemia of hyperphosphatemia was circumvented by the addition of calcium to the infusate, insulin substantially increased the renal tubular reabsorptive capacity for Pi, thereby demonstrating an antiphosphaturic action of insulin independent of PTH. Furthermore, when increased filtered loads of Pi and PTH administration were combined during insulin infusion, TRPi was greater than when PTH was administered alone during similar insulin infusion. When calcium infusion did not accompany Pi loading with a resultant fall in serum calcium, euglycemic hyperinsulinemia did not affect TRPi, indicating abolition of the antiphosphaturic action of insulin by hypocalcemia.