The roles of parathyroid hormone (PTH) in regulating the blood calcium level in mammals.
Control of blood calcium
Because calcium ions (Ca2+) are essential to the normal functioning of all cells, homeostatic control of the level of calcium in the blood is vital.
If the blood Ca2+ level falls substantially, skeletal muscles contract convulsively, a potentially fatal condition.
If the blood Ca2+ level rises substantially, calcium phosphate can form precipitates in body tissues, leading to widespread organ damage.
In mammals, the parathyroid glands, a set of four small structures embedded in the posterior surface of the thyroid, play a major role in blood Ca2+ regulation.
When the blood Ca2+ level falls below a set point of about 10 mg/100 mL, these glands release parathyroid hormone (PTH).
PTH raises the level of blood Ca2+ through direct effects in bones and the kidneys and an indirect effect on the intestines.
In bones,
PTH causes the mineralized matrix to break down, releasing Ca2+ into the blood.
In the kidneys,
PTH directly stimulates the reabsorption of Ca2+ through the renal tubules.
In addition,
PTH indirectly raises the blood Ca2+ level by promoting vitamin D production.
A precursor form of vitamin D is obtained from food or synthesized by skin exposed to sunlight.
Conversion of this precursor to active vitamin D begins in the liver.
PTH acts in the kidney to stimulate the completion of the conversion process.
Vitamin D acts on the intestines, stimulating the uptake of Ca2+ from food.
As the blood Ca2+ level rises, a negative feedback loop inhibits further release of PTH from the parathyroid glands.
The thyroid gland can also contribute to calcium homeostasis.
If the blood Ca2+ level rises above the set point, the thyroid gland releases calcitonin, a hormone that inhibits bone breakdown and enhances Ca2+ excretion by the kidneys.
In fishes, rodents, and some other animals, calcitonin is required for Ca2+ homeostasis.
In humans, however, calcitonin is needed only during the extensive bone growth of childhood.
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