#The mystery of calcium ions in myocytes
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Dm me the answer or post it here but as spoilered messages! The discussion doesn't have to be spoilered, only the final answer 
@eager cedar very easy, ||I'll refer them to a primary physician||
because the cell is funny
so to simply put. when injecting calcium ion into normal muscle cell, will make this muscle cell contract. but doing the same on heart muscle cell will make this heart muscle cell not only contract but also secrete more calcium ion?
yes! more calcium ions will be found in the cytoplasm than just those injected
is that secreated ion or more ion inside the cell?
more ion inside the cell. in the cytoplasm!
would that increased calcium ion. trigger other heart cells to contract and secreat calcium ion?
Idk research that :D although I don't see how it helps you find the answer to this question specifically
he basically confirmed me 
||would it be because striated cells couple dhp with the RyRs for calcium release, whereas cardiac muscle uses calcium to activate calcium release? So the cardiac myocyte has extra calcium since it released some of its own||
Cardiac and striated myocytes probably behave differently and structurally differ
Cardiac muscles are justifiably distinguished
Feeling cardiac myocytes has to do with very regulated ion concentration level for the regulated and regular pulses from the very functional side
Whereas normie normal myocytes would pretty much controlled by voluntary controls from your brain, the cardiac ones has to do on their own, thus the additional regulation of calcium ion concentration when getting the influx from the injection
and which cause other heart cells to contract? and make heart beat?
I'm not sure about the details of intracellular communication between the cardiac myocytes, but the coordination of the whole cardiac muscle (the heart) should be controlled by the brain
I think the question's just talking about a single cardiac myocyte (I could be wrong tho!)
ah shit bio again
But the heart contracts even when disconnected from the central nervous system, coordination between its cells is assured by its autonomous nervous system, right ?
yay bio!
|| Calcium induced calcium release from the SR, calcium binds to RYR on the SR, releasing more calcium into the cytoplasm ||
No, cardiac coordination is present without an ANS, you do have things like heart rate changes though
ooh i didnt know that! makes sense tho in the case of brain-dead patients.
||I had a little idea, the Calcium Induced Calcium Release, by liberation of calcium from sarcoplasmic reticulum by calcium bounding to its receptors on the sarcoplasmic reticulum, but that applies to any striated cell, which isn't what the question is referring to apparently||
||i was a bit confused about that too, but it seems that CICR is primarily used in the cardiac muscle (not sure tho)||
Yes, the heart can contract when isolated from the organism, its default is 120 beatings per minute, the autonomous nervous system (sympathetic/parasympathetic) control its rate, contraction force depending on the organism's needs and situation
It is afaik, but that's no difference in this case ๐คทโโ๏ธ
Ah yeah I just meant the heart's own nervous system, not the sympathetic/parasympathetic
whoa! i always just thought that the heart was controlled by the cns and ans ๐
i just figured it was used more in cardiac than striated, so thats why there was a difference. i dont actually know tho
Actually the autonomous plays a vital role by controlling the heart rate, but yeah it's not necessary for simple contraction
That may be it then
the nervous system always sounds so messy lol
Yeah hahahahha
But it's fascinating aswell !
its dominated by vagal tone, but its generated by the SA node normally
i remember always stressing about my tests on brain function because all the regions seemed so interconnected lol
it definitely is!
||I think the short answer would be the difference in EC coupling (excitation-contraction coupling) AFTER influx of calcium though L-type channles (or in this case from a injection), where in the cardiac myocytes it happens throughout a process called calcium-induced calcium release (CICR), and in the striated myocyes it happens as dihydropyridine receptor (DHPR)-ryanodine receptor (RYR) interactions.||
so, milk ?
||I guess it would be because presence of Ca ions triggers more ions to be released in a certain situation, like there might be more receptors that need to be triggered to cause contraction than injected or the receptors become less sensitive somehow to Ca ions, so the SR releases more to attain a higher amount of Ca ions in the cell...|| However, I am not certain. This is for the most part a guess based on what I think I have understood of what I have read
I need to read more
I don't think bones are in a position to intervene in this short-term situation of cardiac myocytes contraction
Is this an example of positive feedback?
I think positive feedback is hormonal, this is not a hormonal response afaik
So feedback only when hormones are present
Oops I forgot to send the answer here as well
ANSWER
|| The L calcium channel (a dihydropyridine receptor) in the T tubule is connected directly to the RYR receptor on the SR in the striated myocytes. Thus, its mandatory that L receptors get activated so that RYR also gets activated. (a in image)
In smooth and cardiac muscle however, the two aren't connected in their structure (they aren't a continuous structure) and the mechanism is just based on cytoplasmic levels of ionic calcium. (b in image)
Note: The L voltage gated calcium channels are also called dihydropyridine receptors because they have a binding place for dihydropyridine which blocks the activity of these channels. ||
||Cardiac myocytes utilize a specialized mechanism called calcium-induced calcium release (CICR). When calcium is introduced, it not only triggers contraction but also causes the release of additional calcium from internal stores, amplifying the contraction. This mechanism ensures synchronized and efficient heart muscle function.||
oh darn I just realised I was late