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.