Factors affecting parathyroid hormone-induced hypophosphatemia and 32P specific activity in thyroparathyroidectomized rats

Talmage, R.V.; VanderWiel, C.J.; Raneri, D.B.

Calcified Tissue International 27(3): 239-246

1979


ISSN/ISBN: 0171-967X
PMID: 114285
DOI: 10.1007/bf02441192
Accession: 068521015

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Abstract
Plasma changes in Ca, 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 of 45Ca and 32P. Prior to i.v. infusion or hourly injections of PTH (10 mU/g/h), rats were maintained in 1 of 3 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 Ca, 45Ca and 45Ca specific activity (S.A.) produced by PTH was not affected by these dietary conditions. During the experimental (8 h) period, the rate of loss of 32P from plasma in control rats was proportional to the length of the fast. 32P was apparently 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 of 32P from plasma without affecting 32P S.A. values. In rats fasted for only 10 h, PTH produced similar effects on plasma phosphate and plasma 32P values, but also caused a significant fall in plasma 32P S.A. After glucose and calcium lactate treatment, PTH-induced phosphaturia was temporarily lost and the marked hypophosphatemia was replaced with a slight hyperphosphatemia. Plasma 32P values also rose slightly; no effect on 32P S.A. was produced. 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. This phosphate entering plasma is withdrawn primarily from bone fluid and bone.