The effect of Na-EGTA induced hypocalcemia was investigated in chronically parathyroidectomized (PTX) rats. In dietary inorganic phosphorus (Pi) replete animals, reduction in the plasma calcium to 1.37 +/- 0.03 mM at constant filtered loads of Pi had no effect on tubular reabsorption of phosphorus (85 +/- 3 vs. 83 +/- 2 micrograms/ml, NS). In dietary Pi-deprived rats, where an elevation of plasma calcium is a known accompaniment, similar reduction in plasma calcium concentration also failed to alter (89 +/- 2 vs. 90 +/- 2 micrograms/ml, NS) phosphorus reabsorption. Resistance to parathyroid hormone (PTH) in dietary Pi deprivation was confirmed. Super imposition of PTH on EGTA induced hypocalcemia during dietary Pi deprivation, however, resulted in a significant reduction in tubular Pi reabsorption (81 +/- 2 vs. 67 +/- 3 micrograms/ml, p less than 0.05) with full restoration of its phosphaturic action. These changes were unaccompanied by differences in urinary adenosine 3',5'-cyclic phosphate (cAMP). In conclusion, hypocalcemia per se does not alter the renal handling of phosphorus at constant plasma Pi concentrations. The elevation in the plasma calcium associated with dietary Pi deprivation does not contribute importantly to the hypophosphaturia of dietary Pi deprivation. Hypocalcemia, however, abolishes the resistance to PTH observed in Pi deprivation.