The secretion of parathyroid hormone is controlled by the plasma calcium concentrations. Its secretion is stimulated by low calcium concentrations and inhibited by high calcium concentrations. Since parathyroid hormone stimulates the final hy-droxylation step in the formation of 1,25-dihydroxyvitamin D3, a rise in parathyroid hormone results in an increase in production of 1,25-dihydroxyvitamin D3. Low blood calcium can thus be corrected by the effects of increased parathyroid hormone and 1,25-dihydroxyvitamin D3 (fig. 19.22).
It is possible for plasma calcium levels to fall while phosphate levels remain normal. In this case, the increased secretion of parathyroid hormone and the production of 1,25-dihydroxyvitamin D3 that result could abnormally raise phosphate levels while acting to restore normal calcium levels. This is prevented by the inhibition of phosphate reabsorption in the kidneys by parathyroid hormone, so that more phosphate is excreted in the urine (fig. 19.20). In this way, blood calcium can be raised to normal levels without excessively raising blood phosphate concentrations.
Experiments in the 1960s revealed that high blood calcium in dogs may be lowered by a hormone secreted from the thyroid gland. This hormone thus has an effect opposite to that of
Stimulates reabsorption of Ca2+ Inhibits reabsorption
Stimulates intestinal absorption of
Increased plasma Ca2+
■ Figure 19.22 Homeostasis of plasma Ca2+ concentrations. A
negative feedback loop returns low blood Ca2+ concentrations to normal without simultaneously raising blood phosphate levels above normal.
Increased plasma Ca2+
Stimulates excretion of Ca2+ and PO43-
Inhibits dissolution of CaPO4 crystals
Decreased plasma Ca2+
■ Figure 19.23 The negative feedback control of calcitonin secretion. The action of calcitonin is antagonistic to that of parathyroid hormone.
parathyroid hormone and 1,25-dihydroxyvitamin D3. The calcium-lowering hormone, called calcitonin, was found to be secreted by the parafollicular cells, or C cells, of the thyroid. These cells are scattered among the follicular cells that secrete thyroxine.
The secretion of calcitonin is stimulated by high plasma calcium levels and acts to lower calcium levels by (1) inhibiting the activity of osteoclasts, thus reducing bone resorption, and (2) stimulating the urinary excretion of calcium and phosphate by inhibiting their reabsorption in the kidneys (fig. 19.23).
Although it is attractive to think that calcium balance is regulated by the effects of antagonistic hormones, the significance of calcitonin in human physiology remains unclear. Patients who have had their thyroid gland surgically removed (as for thyroid cancer) are not hypercalcemic, as one might expect them to be if calcitonin were needed to lower blood calcium levels. The ability of very large pharmacological doses of calci-tonin to inhibit osteoclast activity and bone resorption, however, is clinically useful in the treatment of Paget's disease, in which osteoclast activity causes softening of bone. It is sometimes also used to treat osteoporosis, as previously described.
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