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  • Identify the origin, target organs and cell types, and physiologic effects of parathyroid hormone.

  • Describe the functions of osteoblasts and osteoclasts in bone remodeling and the factors that regulate their activities.

  • Describe the regulation of parathyroid hormone secretion and the role of the calcium-sensing receptor.

  • Identify the sources of vitamin D and describe the biosynthetic pathway involved in modifying it to its biologically active form.

  • Identify the target organs and cellular mechanisms of action of vitamin D.

  • Describe the negative feedback relationship between parathyroid hormone and the biologically active form of vitamin D.

  • Describe the causes and consequences of excess or deficiency of parathyroid hormone and of vitamin D.

  • Describe the regulation of calcitonin release and the cell of origin and target organs for calcitonin action.

The regulation of plasma Ca2+ levels is critical for normal cell function, neural transmission, membrane stability, bone structure, blood coagulation, and intracellular signaling. This regulation relies on the interactions among parathyroid hormone (PTH) from the parathyroid glands, dietary vitamin D, and calcitonin from the thyroid gland (Figure 5–1). PTH stimulates bone resorption and the release of Ca2+ into the circulation. In the kidney, PTH promotes Ca2+ reabsorption and inorganic phosphate excretion in the urine. In addition, PTH stimulates the hydroxylation of 25-hydroxyvitamin D at the 1-position, leading to the formation of 1,25(OH)2D, the active form of vitamin D (calcitriol). Vitamin D increases intestinal absorption of dietary Ca2+ and facilitates renal reabsorption of filtered Ca2+. In bone, vitamin D increases bone resorption with a resulting increase in the release of Ca2+ into the circulation. Calcitonin counteracts the effects of PTH by inhibiting bone resorption and increasing renal Ca2+ excretion. The overall result of the interactions among PTH, vitamin D, and calcitonin is the maintenance of normal plasma Ca2+ concentrations.

Figure 5–1.

Negative feedback regulation of parathyroid hormone (PTH) release. A sudden decrease in Ca2+ stimulates the release of PTH from the parathyroid gland. PTH increases the activity of 1α-hydroxylase in the kidney, leading to increased activation of vitamin D. In addition, PTH increases the renal reabsorption of Ca2+ and decreases the reabsorption of inorganic phosphate (Pi). In bone, PTH stimulates bone resorption, increasing the plasma Ca2+ levels. The elevations in vitamin D and plasma Ca2+ levels exert negative feedback inhibition of PTH release. Elevations in plasma Pi levels stimulate the release of PTH.


The parathyroid glands are pea-sized glands located at the top and bottom posterior borders of the lateral lobes of the thyroid gland. The glands are richly vascularized and consist primarily of chief cells, with a thin capsule of connective tissue that divides the gland into lobules. The chief cells synthesize and secrete PTH, a polypeptide hormone that ...

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