Calcium ions

From The School of Biomedical Sciences Wiki
(Difference between revisions)
Jump to: navigation, search
(Cleaned up the references.)
Line 11: Line 11:
 
#Matrix vesicles found in the [[Osteoblasts|osteoblasts]] contain alkaline phosphatase.
 
#Matrix vesicles found in the [[Osteoblasts|osteoblasts]] contain alkaline phosphatase.
  
If there is a calcium deficiency in the [[Blood|blood]], mineralization does not complete causing a disease called [[Osteomalacia|osteomalacia]]. This causes the bone to soften and become more vulnerable to damage leading to rickets or other bone deformities <ref>Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref>.  
+
If there is a calcium deficiency in the [[Blood|blood]], mineralization does not complete causing a disease called [[Osteomalacia|osteomalacia]]. This causes the bone to soften and become more vulnerable to damage leading to rickets or other bone deformities<ref>Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref>.  
  
 
==== Parathyroid Hormone  ====
 
==== Parathyroid Hormone  ====
  
[[Parathyroid gland|Parathyroid glands]], located in the region of the neck, release the hormone parathormone which maintains the calcium concentration in the blood. In order to increase the concentration it mobilizes the calcium stored in mineralized bone&nbsp;<ref>Lowe, J. and Stevens, A. (2005:279) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref> by stimulating osteoclastic activity<ref>Lowe, J. and Stevens, A. (2005:261) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref>. This works by reducing the loss of calcium ions in the kidney and by increasing the reabsorption of the ion into the small intestine.  
+
[[Parathyroid gland|Parathyroid glands]], located in the region of the neck, release the hormone parathormone which maintains the calcium concentration in the blood. In order to increase the concentration it mobilizes the calcium stored in mineralized bone<ref>Lowe, J. and Stevens, A. (2005:279) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref> by stimulating osteoclastic activity<ref>Lowe, J. and Stevens, A. (2005:261) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref>. This works by reducing the loss of calcium ions in the kidney and by increasing the reabsorption of the ion into the small intestine.  
  
 
When calcium ions levels are persistently low the constant activity of [[Parathyroid glands|parathyroid glands]] cause them to swell. This swelling is called parathyroid hyperplasia. Additionally, an over-secretion of parathormone brings about excessive damage to the bone and a surplus of calcium in the blood.  
 
When calcium ions levels are persistently low the constant activity of [[Parathyroid glands|parathyroid glands]] cause them to swell. This swelling is called parathyroid hyperplasia. Additionally, an over-secretion of parathormone brings about excessive damage to the bone and a surplus of calcium in the blood.  

Revision as of 19:27, 28 November 2017

Contents

Importance of Calcium Ions

Ca2+ ions play an important role in muscle contraction by creating interactions between the proteins, myosin and actin. The Ca2+ ions bind to the C component of the actin filament, which exposes the binding site for the myosin head to bind to in order to stimulate a muscle contraction[1].

Bone Mineralization

Bone rigidity is partially due to a salt in its osteoid matrix which consists of calcium and phosphate ions. If the ion concentrations are above the threshold value then bone mineralization will occur. In order to maintain the ion concentrations:

  1. Osteocalcin, a glycoprotein, binds to calcium ions within the osteoid.
  2. Alkalin phosphatase, an enzyme, increases the calcium and phosphate ion concentration.
  3. Matrix vesicles found in the osteoblasts contain alkaline phosphatase.

If there is a calcium deficiency in the blood, mineralization does not complete causing a disease called osteomalacia. This causes the bone to soften and become more vulnerable to damage leading to rickets or other bone deformities[2].

Parathyroid Hormone

Parathyroid glands, located in the region of the neck, release the hormone parathormone which maintains the calcium concentration in the blood. In order to increase the concentration it mobilizes the calcium stored in mineralized bone[3] by stimulating osteoclastic activity[4]. This works by reducing the loss of calcium ions in the kidney and by increasing the reabsorption of the ion into the small intestine.

When calcium ions levels are persistently low the constant activity of parathyroid glands cause them to swell. This swelling is called parathyroid hyperplasia. Additionally, an over-secretion of parathormone brings about excessive damage to the bone and a surplus of calcium in the blood.

Muscle Contraction

Skeletal Muscle Cells

During muscle contraction, high concentrations of calcium are required to displace troponin and reveal the active site at which myosin binds to for the power stroke. Calcium is released from the sarcoplasmic reticulum through calcium ion channels when the membrane of the T-tubular system is excited. It binds to Troponin C causing it to conform, hence permitting the myosin head to latch onto the actin filament, onsetting muscle contraction[5].

Cardiac Muscle

Similarly to skeletal muscles, the contraction of cardiac muscles is regulated by the concentration of calcium ions. However, some main differences in contraction mechanisms are that:

  1. The T-tubular system in cardiac muscles has much greater invaginations on the cell surface.
  2. The sarcoplasmic reticulum is much less complex in comparison to that in the skeletal muscle[6].

References

  1. https://teaching.ncl.ac.uk/bms/wiki/index.php/Ca2%2B_ions
  2. Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
  3. Lowe, J. and Stevens, A. (2005:279) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
  4. Lowe, J. and Stevens, A. (2005:261) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
  5. Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
  6. Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
Personal tools
Namespaces
Variants
Actions
Navigation
Toolbox