Calcium homeostasis: parathyroid hormone, vitamin D and calcitonin

What it is

A fall in serum Ca2+ levels stimulates the parathyroid glands, and PTH secretion follows. PTH then acts at two sites. On bone it raises osteoclast resorption. In the kidney it turns on 1a-OHase, so 1a,25(OH)2D3 formation rises, calcium excretion falls and PO4 excretion rises. It is the raised 1a,25(OH)2D3, and not PTH itself, that acts on the intestine, where Ca2+ absorption from food rises; the same 1a,25(OH)2D3 also acts back on the osteoclasts, so the bone is acted on twice. The result is Ca2+ release into serum, and homeostasis follows, since high serum Ca2+ levels inhibit the parathyroid glands. High serum Ca2+ levels also act on the thyroid gland, which gives calcitonin. Calcitonin leads to Ca2+ deposition in bones through the osteoblast, and stops bone resorption at the mature osteoclast. Calcitonin also acts on the kidney, and there Ca2+ uptake falls, with clearance through urine. That same 1a,25(OH)2D3 meets 24-OHase in the kidney, which forms 24(R),25(OH)2D, and it too ends in clearance through urine.