Calcium ions: Difference between revisions
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== | === Importance of Calcium Ions === | ||
==== Bone Mineralization ==== | ==== Bone Mineralization ==== | ||
Bone rigidity is partially due to a salt in it's 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: | Bone rigidity is partially due to a salt in it's osteoid matrix which consists of [[calcium|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: | ||
#[[Osteocalcin|Osteocalcin]], a [[glycoprotein|glycoprotein]], binds to calcium ions within the osteoid. | |||
#Alkalin phosphatase, an [[enzyme|enzyme]], increases the calcium and phosphate ion concentration. | |||
#Matrix vesicles found in the osteoblasts contain alkalin 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 deformaties <ref>Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref>.<br> | |||
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 deformaties | |||
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==== Parathyroid Hormone ==== | ==== Parathyroid Hormone ==== | ||
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<span style="line-height: 1.5em;">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. </span><br> | <span style="line-height: 1.5em;">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. </span><br> | ||
When calcium ions levels are persistently low the constant activity of parathyroid glands cause them to swell. This swelling is called parathyroid hyperlasia. 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 hyperlasia. Additionally, an over-secretion of parathormone brings about excessive damage to the bone and a surplus of calcium in the blood. <br> | ||
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==== Muscle Contraction ==== | ==== Muscle Contraction ==== | ||
===== Skeletal Muscle Cells ===== | ===== 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. <ref>Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref> | During muscle contraction high concentrations of calcium are required to displace [[troponin|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|Troponin C]] causing it to conform, hence permitting the [[myosin|myosin]] head to latch onto the [[actin|actin]] filament, onsetting muscle contraction. <ref>Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref><br> | ||
===== Cardiac Muscle ===== | |||
===== 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: | 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: | ||
#The T-tubular system in cardiac muscles have much greater invaginations on the cell surface. | |||
#The [[sarcoplasmic reticulum|sarcoplasmic reticulum]] is much less complex in comparison to that in the skeletal muscle. <ref>Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.</ref> | |||
=== References === | |||
<references /><br> | <references /><br> |
Revision as of 05:52, 29 November 2013
Importance of Calcium Ions
Bone Mineralization
Bone rigidity is partially due to a salt in it's 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:
- Osteocalcin, a glycoprotein, binds to calcium ions within the osteoid.
- Alkalin phosphatase, an enzyme, increases the calcium and phosphate ion concentration.
- Matrix vesicles found in the osteoblasts contain alkalin 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 deformaties [1].
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"[2] by "stimulating osteoclastic activity"[3]. 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 hyperlasia. 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. [4]
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:
- The T-tubular system in cardiac muscles have much greater invaginations on the cell surface.
- The sarcoplasmic reticulum is much less complex in comparison to that in the skeletal muscle. [5]
References
- ↑ Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
- ↑ Lowe, J. and Stevens, A. (2005:279) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
- ↑ Lowe, J. and Stevens, A. (2005:261) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
- ↑ Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
- ↑ Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.