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Studies on the mechanisms underlying the transfer of calcium and phosphate from bone to blood

Thesis/Dissertation ·
DOI:https://doi.org/10.2172/6802123· OSTI ID:6802123
 [1]
  1. Univ. of Rochester, NY (United States)
The skeleton is recognized as a crucial organ in the minute-to-minute regulation of the blood levels of calcium and phosphate. The fluxes of calcium and phosphate to and from bone greatly exceed the entry and exit of these ions occurring in the intestine and kidneys. Parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3 are known to influence the transfer of calcium and phosphate from bone to blood. Three mechanisms have been proposed to explain the hormonal control of the calcium and phosphate effluxes from bone. The concept of a bone membrane maintaining a distinct bone extracellular fluid composition has led to the pump and pH gradient theories. An alternate solubilizer theory proposes that bone cells secrete a substance which increases the solubility of the bone mineral. The bone membrane concept was originally proposed to explain the presence of the apparent anomalously high concentrations of potassium in the bone extracellular fluid. However, the available evidence does not allow an unambiguous decision concerning the presence of a bone membrane. Calvarial lactate production was unaltered by 1,25-(OH)2D3 treatment and consequently 1,25-(OH)2D3 does not appear to promote the mobilization of bone mineral through a lactate-mediated pH gradient mechanism. 1,25-(OH)2D3 did increase the solubility of non-vital bone, clearly demonstrating that the solubilizer mechanism is at least partially responsible for the mobilization of bone mineral and the regulation of blood levels of calcium and phosphate. Vitamin D-deficient female rats fed a 0.2% calcium, 0.4% phosphorous diet and supplemented with daily injections of 0.75 pmole of 1,25-(OH)2D3 were shown to be capable of bearing young. When the injections of 1,25-(OH)2D3 were terminated at delivery, the dams and pups showed signs of vitamin D deficiency approximately one week later.
Research Organization:
Univ. of Rochester, NY (United States). Dept. of Radiation Biology and Biophysics
Sponsoring Organization:
USDOE
DOE Contract Number:
EY-76-C-02-3490
OSTI ID:
6802123
Report Number(s):
UR--3490-1468
Country of Publication:
United States
Language:
English