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idagr811
Forum Newbie Topics: 2 Posts: 3 |
In hypocalcemia, why is there tetani? shouldn't that be the response to HYPERcalcemia?
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suvi21
| Forum Junior Topics: 6 Posts: 81
Intern_doc, I can see why idgr is asking. I agree with your explanation, but if you look at the cellular machanism, it seems like when you have less ECF Ca, less should be able to get into the cells and therefore cells should be less depolarized... less excitable. Instead, they are more excitable; I find this a paradox too. Any thoughts on that?
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idagr811
| Forum Newbie Topics: 2 Posts: 3
Yes, that's exactly what I mean, suvi21.
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mash
| Forum Guru Topics: 147 Posts: 1299
Skeletal muscle can contract in the absence of extracellular calcium, and skeletal S.R, shows depolarisation-induced calcium release source of calcium in sk ms contraction is sar reticulum no extracellular ca is involved. in tetanic contractions inside of cell is saturated with free calcium which is frm SR. so, all cross bridges dat can cycle with sites on actin will be continuously cycling.. and one thing more, surface mem of sk ms does not ve voltage gated ca channels. as interndoc has said dat the nervous system becomes increasingly excitable, and nerves discharge spontaneously, sending impulses to skeletal muscles and causing spasmodic contractions.
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mani
| Forum Guru  Topics: 104 Posts: 1400
thats exactly true mash! and this is what the differencee is in the xcitation-contraction coupling mechanism in skeletal and cardiac muscle. skeletal muscle is totally independent of extracellular calcium for contraction. only way extracellular calcium affects the skeletal muscle contraction is by increasing excitability of nervous tissue. normally some of the Na channels are "plugged" by Ca and thus are unavailable. in hypocalcemia these pluggeed channels also become available for AP. hence excitability of nervous tissue is increased----> tetany
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suvi21
| Forum Junior Topics: 6 Posts: 81
Thanks mash, for the nice explanation. However, I was referring to neuronal depolarization, not skeletal muscle depolarization. For neuronal depolarization (mainly Na) and subsequent docking of vesicles to release neurotransmitter ( Ca) at the MEP, Ca is reqiured. So, my Q is, if ECF Ca is reduced, how does the neurons become hyperexcitable?
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mani
| Forum Guru Topics: 104 Posts: 1400
suvi i hope my explanation helps
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mash
| Forum Guru Topics: 147 Posts: 1299
hypocalcemia decreases the threshold potential for activation of voltage-gated Na+ channels..
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suvi21
| Forum Junior Topics: 6 Posts: 81
Yes Mani and mash, that explains, thanks :P ; now I feel better about tetany :wink:
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Sakaki-
| Forum Senior Topics: 1 Posts: 238
(Just something to add): The membrane contains acidic groups in the mrmbane phospholipids and proteins (including the sialic acid carbohydrate groups); the positively charged calcium neutralizes these surface charges and makes the field within the membrane steeper (a greater potential gradient), reducing the gating effect of depolarization and thereby increasing the threshold potential in cases of hypercalcemia.
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