Biological functions of calcium
The overwhelming majority of calcium acts as a structural component of bone tissue. The remaining one percent circulates in the extracellular fluid as dissolved Ca2+ ions or binds to blood proteins. This small pool performs vital tasks:
- Initiates muscle contraction.
- Regulates cell membrane permeability to potassium ions and sodium conductance.
- Controls the operation of various ion pumps.
- Ensures hormone secretion.
- Takes an obligatory part in the blood coagulation cascade.
- Serves as a crucial mediator (second messenger) for intracellular signal transduction.
Main homeostatic regulators
The concentration of calcium and phosphates is regulated by three hormones that act on target organs:
| Hormone | Site of synthesis | Mechanism and effects |
|---|---|---|
| Parathyroid hormone (PTH) | Parathyroid glands | Secreted when Ca2+ decreases. Via osteoblast adenylate cyclase, it activates osteoclasts (calcium leaching). In the kidneys, it enhances calcium reabsorption and inhibits phosphate reabsorption. |
| Calcitriol | Kidneys | Increases calcium and phosphate absorption in the intestine. Regulates transcription in the nucleus. |
| Calcitonin | Thyroid C cells | Released during hypercalcemia. Suppresses osteoclasts (inhibits bone resorption) and enhances the urinary excretion of ions. |
Vitamin D metabolism
The synthesis of the active hormone, calcitriol, occurs in several strict stages involving different organs:
- Precursor formation: Cholesterol is converted into 7-dehydrocholesterol (containing a double bond between carbon atoms 7 and 8 in ring B).
- Cutaneous stage (photolysis): In the epidermis, under the influence of ultraviolet light, a non-enzymatic cleavage of the bond between atoms 9 and 10 occurs. Cholecalciferol (vitamin D3) is formed.
- Hepatic stage: The enzyme 25-hydroxylase attaches an OH group to the 25th carbon atom. This yields the transport form, calcidiol.
- Renal stage: In the mitochondria of the proximal tubules, under the action of 1-alpha-hydroxylase, the active form—calcitriol (1,25-dihydroxycholecalciferol)—is synthesized.
Clinical aspects: hyper- and hypoparathyroidism
In primary hyperparathyroidism (e.g., due to an adenoma), excess PTH causes massive bone resorption. Hypercalcemia ensues, which reduces neuromuscular excitability, causing muscle weakness and intestinal atony (constipation). Excess calcium is filtered into the urine (hypercalciuria), which, together with phosphaturia, leads to kidney stone formation (renal colic).
In hypoparathyroidism (after removal or damage to the parathyroid glands), PTH deficiency leads to a drop in blood calcium levels. This sharply increases neuromuscular excitability. The patient develops cramps and tetany, up to life-threatening laryngospasm.
Vitamin D dysfunction and rickets
Calcitriol binds to the intracellular VDR receptor, enters the nucleus, and triggers the synthesis of calbindin, a protein required for calcium absorption in the intestine. When failures occur at any stage, rickets or osteomalacia develops.
Main causes of deficiency:
- Dietary deficiency or lack of UV light.
- Intestinal malabsorption.
- Liver diseases (impaired 25-hydroxylation).
- Kidney diseases (impaired 1-alpha-hydroxylation).
- Genetic defects in VDR receptors.
Briefly: answers to topical questions
Which specific blood plasma proteins does calcium bind to?
Calcium binds to blood plasma albumins.
These proteins are simple acidic proteins and perform a vital transport function. Interaction features:
- Albumins transport calcium ions in the bloodstream alongside fatty acids and bilirubin.
- When the concentration of $H^+$ ions decreases (alkalosis), the binding of $Ca^{2+}$ by albumins increases.
- Such binding reduces the active fraction of ionized calcium in plasma, which can lead to hyperventilation tetany.
What is the difference between primary and secondary hyperparathyroidism?
The main difference lies in the cause of elevated PTH and the blood calcium level.
| Characteristic | Primary hyperparathyroidism | Secondary hyperparathyroidism |
|---|---|---|
| Cause | Parathyroid adenoma | Response to CKD abnormalities; also compensatory elevation of PTH in vitamin D deficiency |
| Calcium level | Hypercalcemia | In secondary hyperparathyroidism due to CKD, calcium levels remain low; in vitamin D deficiency, there is a risk of hypocalcemia |
| Pathogenesis | Parathyroid hypersecretion → bone tissue resorption, Ca²⁺ release into the blood, hypercalcemia | In CKD, high phosphate levels and decreased active vitamin D stimulate the parathyroid glands; in D₃ deficiency, impaired calcium absorption triggers secondary hyperparathyroidism |
Parathyroid hormone RAISES blood calcium (extracts it from bone), while calcitoTONIN pulls it DOWN (keeps it in bone and excretes it via urine).
Class and exam questions
Why do bones break down in vitamin D deficiency?
Due to a lack of the vitamin, calcium absorption in the intestine decreases. The threat of hypocalcemia develops, to which the body responds with secondary hyperparathyroidism—elevated parathyroid hormone begins to break down bone hydroxyapatites to return calcium to the blood.
How does parathyroid hormone affect the kidneys?
Parathyroid hormone stimulates calcium reabsorption in the distal renal tubules, returning it to the blood, while simultaneously decreasing phosphate reabsorption and enhancing its excretion in the urine.
What causes hypercalciuria?
Increased urinary calcium excretion occurs in hyperparathyroidism, vitamin D overdose, metabolic acidosis, bone metastases, or due to idiopathic tubular reabsorption disorders.
What else to study on this topic
- Mechanism of osteoclast activation via osteoblast receptors
- Role of cAMP and inositol trisphosphate (IP3) in PTH signal transduction
- Symptoms and compensation of metabolic acidosis via bone tissue
- Vitamin D-dependent rickets: molecular genetics of VDR receptors
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