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Parathyroid hormone (PTH), or parathormone, is secreted by the parathyroid glands as a polypeptide containing 84 amino acids. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration.
PTH acts to increase the concentration of calcium in the blood by acting upon parathyroid hormone receptor in three parts of the body: PTH half-life is approximately 4 minutes.
Regulation of serum calcium
Parathyroid hormone regulates serum calcium levels through its effects on the following tissues:
bone | It enhances the release of calcium from the large reservoir contained in the bones.
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Encyclopedia
Parathyroid hormone (PTH), or parathormone, is secreted by the parathyroid glands as a polypeptide containing 84 amino acids. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration.
PTH acts to increase the concentration of calcium in the blood by acting upon parathyroid hormone receptor in three parts of the body: PTH half-life is approximately 4 minutes.
Function
Regulation of serum calcium
Parathyroid hormone regulates serum calcium levels through its effects on the following tissues:
| Region | Effect
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| bone | It enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL, which can bind to osteoclast precursors containing RANK, a receptor for RANKL. The binding of RANKL to RANK stimulates these precursors to fuse, forming new osteoclasts which ultimately enhances the resorption of bone.
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| kidney | It enhances active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. As bone is degraded both calcium and phosphate are released. It also greatly increases the excretion of Phosphate, with a net loss in plasma Phosphate concentration. By increasing the calcium:phosphate ratio more calcium is therefore free in the circulation.
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| intestine via kidney | It enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-Hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D affects the absorption of calcium (as Ca2+ ions) by the intestine via calbindin. |
PTH was one of the first hormones to be shown to use the G-protein, adenylyl cyclase second messenger system.
Normal total plasma calcium level ranges from 8.5 to 10.2 mg/dL (2.12 mmol/L to 2.55 mmol/L).
Regulation of serum phosphate
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney which means more phosphate is excreted through the urine.
However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, which is mediated by an increase in activated vitamin D, the absorption of phosphate is not as dependent on vitamin D as is that of calcium. The end result is a small net drop in the serum concentration of phosphate.
Vitamin D synthesis
PTH increases the activity of 1-a-hydroxylase enzyme, which converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, the active form of vitamin D.
Regulation of PTH secretion
Secretion of parathyroid hormone is chiefly controlled by serum [Ca2+] through negative feedback, which is achieved by the activation of calcium-sensing receptors located on parathyroid cells. The second messenger of parathyroid chief cells responsible for PTH secretion is cAMP.
Stimulators
- Decreased serum [Ca2+].
- Mild decreases in serum [Mg2+].
Inhibitors
- Increased serum [Ca2+].
- Severe decreases in serum [Mg2+], which also produces symptoms of hypoparathyroidism (such as hypocalcemia).
Clinical significance
- A high level of PTH in the blood is known as hyperparathyroidism.
- If the cause is in the parathyroid gland it is called primary hyperparathyroidism. The causes are parathyroid adenoma, parathyroid hyperplasia and parathyroid cancer.
- If the cause is outside the gland, it is known as secondary hyperparathyroidism. This can occur in chronic renal failure. In secondary hyperparathyroidism, serum Calcium levels are decreased, which causes the hypersecretion of PTH from the parathyroid glands. PTH acts on the proximal tubules in the kidney to decrease reabsorption of Phosphate (increasing its excretion in urine, decreasing its serum concentration). NOTE: however, in chronic renal failure, because the kidneys are failing they are unable to excrete phosphate in the urine, so in this case of secondary hyperparathyroidism, serum calcium will be decreased, but serum phosphate will be increased.
- A low level of PTH in the blood is known as hypoparathyroidism. Causes include surgical misadventure (eg inadvertent removal during routine thyroid surgery), autoimmune disorder, and inborn errors of metabolism.
Measurement
PTH can be measured in the blood in several different forms: intact PTH; N-terminal PTH; mid-molecule PTH, and C-terminal PTH, and different tests are used in different clinical situations.
The average PTH level is 10-60 pg/ml.
See also
Further reading
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