Factors affecting parathyroid hormone-induced hypophosphatemia and³²P specific activity in thyroparathyroidectomized rats

Summary

Plasma changes in calcium, phosphate, and their radionuclides were studied in thyroparathyroidectomized (TPTX) rats treated with parathyroid hormone (PTH) for 8 h, this treatment starting 10 h after injection of⁴⁵Ca and³²P. Prior to intravenous infusion or hourly injections of PTH (10 mU/g/h), rats were maintained in one of three ways: on an extended fast (24 h); on a partial fast (10 h); or provided with 10% glucose and 1% calcium lactate overnight as a substitution for solid food. The pattern of change for plasma calcium,⁴⁵Ca, and⁴⁵Ca specific activity (S.A.) produced by PTH was not affected by these dietary conditions. The changes in phosphate were as follows: During the experimental (8 h) period, the rate of loss of³²P from plasma in control rats was proportional to the length of the fast. This suggests that³²P was released into plasma during the experimental period proportional to the ready availability of soft tissue glucose. In rats on an extended fast, PTH was phosphaturic, hypophosphatemic, and increased the rate of loss of³²P from plasma without affecting³²P S.A. values. In rats fasted for only 10 h, PTH produced similar effects on plasma phosphate and plasma³²P values, but also caused a significant fall in plasma³²P S.A. After glucose and calcium lactate treatment, PTH-induced phosphaturia was temporarily lost and the marked hypophosphatemia was replaced with a slight hyperphosphatemia. Plasma³²P values also rose slightly; therefore, no effect on³²P S.A. was produced. It is concluded from these studies that as the result of the phosphaturia caused by PTH, the hypophosphatemia which is produced automatically changes the phosphate gradient between various body compartments, causing phosphate entry into plasma. The authors postulate that this phosphate entering plasma is withdrawn primarily from bone fluid and bone.