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Calcium Homeostasis

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Calcium homeostasis is the set of physiological processes that keeps the concentration of calcium in extracellular fluid, especially ionized calcium in blood, within a narrow range. This regulation is essential because calcium is required for functions including nerve transmission, muscle contraction, blood coagulation, cellular signaling, and secretion. Although about 99 percent of body calcium is stored in the skeleton, the much smaller extracellular pool is tightly regulated .1,2

The principal hormonal regulators are parathyroid hormone (PTH) and calcitriol, the active hormonal form of vitamin D. When ionized calcium falls, reduced activation of calcium-sensing receptors in the parathyroid glands promotes increased PTH secretion. PTH increases renal calcium reabsorption, promotes processes that can mobilize calcium from bone, and stimulates the kidney to produce more calcitriol. Calcitriol increases intestinal calcium absorption, helping restore extracellular calcium toward its regulated range .1,2

When extracellular calcium rises, PTH secretion decreases, reducing PTH-driven renal calcium conservation and calcitriol production. Bone, kidneys, and the gastrointestinal tract therefore act together as major sites of calcium exchange and regulation. Calcitonin can influence bone resorption but has a comparatively minor role in normal calcium homeostasis in humans .1

Calcium homeostasis is distinct from calcium balance or total body calcium stores. Blood calcium can remain within its normal physiological range even when dietary calcium intake is insufficient because regulatory mechanisms can mobilize calcium from skeletal stores. Maintaining normal blood calcium therefore does not necessarily indicate that bone calcium stores are adequate .1,2

References

  1. Shaker JL, Deftos L Calcium and Phosphate Homeostasis. Endotext [Internet]. 2023. About this source Original source
  2. Institute of Medicine Dietary Reference Intakes for Calcium and Vitamin D: Ross AC, Taylor CL, Yaktine AL, Del Valle HB, editors. 2011. About this source DOI

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