Guntupalli J, Bourke E
Department of Medicine, Veterans Administration Medical Center, Atlanta, Ga.
Miner Electrolyte Metab. 1989;15(4):201-8.
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.
在长期甲状旁腺切除（PTX）的大鼠中研究了Na-EGTA诱导的低钙血症的影响。在饮食中无机磷（Pi）充足的动物中，在Pi滤过负荷恒定的情况下，血浆钙降至1.37±0.03 mM对肾小管磷重吸收没有影响（85±3对83±2微克/毫升，无显著性差异）。在饮食中Pi缺乏的大鼠中，已知会伴随血浆钙升高，类似的血浆钙浓度降低也未能改变（89±2对90±2微克/毫升，无显著性差异）磷重吸收。证实了饮食中Pi缺乏时对甲状旁腺激素（PTH）的抵抗。然而，在饮食中Pi缺乏期间，在EGTA诱导的低钙血症基础上叠加PTH，导致肾小管Pi重吸收显著降低（81±2对67±3微克/毫升，p<0.05），其磷尿作用完全恢复。这些变化并未伴随尿腺苷3',5'-环磷酸（cAMP）的差异。总之，在血浆Pi浓度恒定的情况下，低钙血症本身不会改变肾脏对磷的处理。与饮食中Pi缺乏相关的血浆钙升高对饮食中Pi缺乏导致的低磷尿症没有重要贡献。然而，低钙血症消除了在Pi缺乏时观察到的对PTH的抵抗。
