parathyroid hormone?

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superduper12

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MCAT -

my textbook says that parathyroid hormone raises blood calcium.

it then says that a lack of PTH causes blood calcium levels to drop leading to convulsion contractions of skeletal muscle...causing tetany.

can anyone relate this to muscle contraction and how Ca2+ ions are in the sarcoplasmic reticulum (which is inside the cell).

I guess I don't understand how tetany is caused...do the Ca2+ ions leave the sarcoplasmic reticulum and enter the blood in an effort to raise Ca2+ levels of the blood? ...and as a sideeffect there is more Ca2+ in the cytosol?
 
The sarcoplasmic reticulum is specialized to sequester and release Ca2+. There are active transporters in the sarcoplasmic reticulum that remove Ca2+ from the sarcoplasm. When an action potential travels down the T-tubular network, it depolarizes the sarcoplasmic reticulum and causes the voltage-gated Ca2+ channels to open. This allows Ca2+ to rush out of the sarcoplasmic reticulum in to the sarcoplasm and an increase in Ca2+ concentration. Ca2+ binds to troponin and undergoes a conformational change, which moves tropomyosin out of the way so that the myosin heads can attach to actin and cause a contraction.

So obviously, a lack of PTH will decrease the Ca2+ concentration and there will be no Ca2+ to bind to troponin. Troponin will not change conformation to move the tropomyosin out of the way and there will be no muscle contraction because myosin heads are not capable of binding to actin. Remember that tropomyosin is always attached to the myosin binding site and must be moved by troponin in order to expose the binding sites for myosin heads.
 
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alright here is what I have got, please correct me if I am wrong.

PTH normally raises blood calcium due to
- to the increased osteoclast activity in the bone and
- it activates vitamin D which stimulates Ca2+ absorption from the intestines

So when PTH is low it reduces blood calcium. Reduced calcium in the synapse changes the voltage for the voltage gated sodium channels. The voltage gated sodium channels are sensitive to voltage changes. Thus they can now depolarize more easily. So sodium enters the cell more easily and we get more action potentials which reach the muscle causing more muscle contraction, tetany and muscle spasm.

Then it follows to what dodjie16 said:
"The sarcoplasmic reticulum is specialized to sequester and release Ca2+. There are active transporters in the sarcoplasmic reticulum that remove Ca2+ from the sarcoplasm. When an action potential travels down the T-tubular network, it depolarizes the sarcoplasmic reticulum and causes the voltage-gated Ca2+ channels to open. This allows Ca2+ to rush out of the sarcoplasmic reticulum in to the sarcoplasm and an increase in Ca2+ concentration. Ca2+ binds to troponin and undergoes a conformational change, which moves tropomyosin out of the way so that the myosin heads can attach to actin and cause a contraction."
 
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