Abstract
The interactions of parathyroid hormone (PTH), calcitonin (CT) and vitamin D in mineral and skeletal homeostasis are discussed. Evidence is presented that not only does PTH control the renal synthesis of 1,25-dihydroxyvitamin D 3 (1,25-(OH) 2D 3), the biologically active form of vitamin D 3, but also that 1,25-(OH) 2D 3 acts as a feedback inhibitor of PTH secretion. Thus, the plasma concentrations of both 1,25-(OH) 2D 3 and calcium are controlled by the actions of PTH, and both of these metabolites operate as feedback inhibitors of PTH secretion. At the level of bone cell function, present evidence indicates that both PTH and CT influence the size of the osteoclast and osteoblast cell pools and the respective activities of the cells in these pools: PTH increases the size of the osteoclast pool and the activity of the cells in this pool; CT has the opposite effects; and 1,25-(OH) 2D 3 seems to increase the activity of these cells as well as those in the osteoblast pool without altering the size of these pools. These different effects are interpreted in terms of the actions of these three hormonal agents on the concentration of three second messengers, cyclic adenosine monophosphate (AMP), calcium ion and monohydrogen phosphate, within the cell.
Published Version
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