Vascular smooth muscle contraction and cardiac muscle contraction

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white_o
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Can anyone help me out? I'm confused as to the following:

Normally, in vascular smooth muscle or cardiac muscle, calcium enters cells via L-type voltage-gated calcium channels, which goes on to activate Ryanodine receptors which then stimulate the opening of SERCA pumps to facilitate Calcium-induced calcium release from the sarcoplasmic reticulum. As well as this Gq also facilitates the release of Calcium from the SR via IP3.

Then is it that in both cardiac and smooth muscle, the calcium first binds to calmodulin, therefore activating myosin light chain kinase which phosphorylates myosin, allowing calcium to then bind to actin and so on to cause the contraction??

Pls help!
Thanks
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bobby147
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First paragraph is right .Second paragraph is right only for smooth muscle contraction. Calmodulin and myosin light chain kinase aren't involved in cardiac muscle contraction.

Cardiac muscle: Calcium enters the cells via L Type voltage gated channels located in the T-tubules during depolarisation.This calcium then binds to ryanodine receptors on the sarcoplasmic reticulum,which releases large amounts of calcium stored in the sarcoplasmic reticulum. This ability of phenomena of calcium from depolarisation resulting in a large release of intracellular calcium is called calcium induced calcium release.

The calcium binds to troponin (you might see troponin C in some books, thats the part of troponin that binds calcium).Troponin is bound to tropomyosin which covers myosin binding sites on actin. Calcium binding to troponin induces a conformational change in tropronin-tropomyosin complex which moves tropomyosin and leaves the myosin binding sites exposed,so myosin can bind now to actin .


Vacular smooth muscle: This one is more interesting at least in how the increase in calcium occurs, since it can occur through either L type voltage gated channels activated by depolarisation or SR release of calcium via IP3 receptors by Gq stimulated by ligands like you said.So unlike cardiac and skeletal cells, you don't have to depolarise vascular smooth cells to contract them thanks to the Gq mechanism.

The calcium binds to calmodulin and forms a calcium-calmodulin complex,which activates myosin chain light chain kinase(MCLK).
MCLK can now phosphorylate myosin light chains, which then form cross bridge formations with actin filaments ,leading to smooth muscle contraction.
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white_o
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(Original post by bobby147)
First paragraph is right .Second paragraph is right only for smooth muscle contraction. Calmodulin and myosin light chain kinase aren't involved in cardiac muscle contraction.

Cardiac muscle: Calcium enters the cells via L Type voltage gated channels located in the T-tubules during depolarisation.This calcium then binds to ryanodine receptors on the sarcoplasmic reticulum,which releases large amounts of calcium stored in the sarcoplasmic reticulum. This ability of phenomena of calcium from depolarisation resulting in a large release of intracellular calcium is called calcium induced calcium release.

The calcium binds to troponin (you might see troponin C in some books, thats the part of troponin that binds calcium).Troponin is bound to tropomyosin which covers myosin binding sites on actin. Calcium binding to troponin induces a conformational change in tropronin-tropomyosin complex which moves tropomyosin and leaves the myosin binding sites exposed,so myosin can bind now to actin .


Vacular smooth muscle: This one is more interesting at least in how the increase in calcium occurs, since it can occur through either L type voltage gated channels activated by depolarisation or SR release of calcium via IP3 receptors by Gq stimulated by ligands like you said.So unlike cardiac and skeletal cells, you don't have to depolarise vascular smooth cells to contract them thanks to the Gq mechanism.

The calcium binds to calmodulin and forms a calcium-calmodulin complex,which activates myosin chain light chain kinase(MCLK).
MCLK can now phosphorylate myosin light chains, which then form cross bridge formations with actin filaments ,leading to smooth muscle contraction.
Thank you so much! So in cardiac muscle it's only via Ryanodine receptors, not IP3, and in vascular smooth muscle it's only via IP3 but not Ryanodine receptors?
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bobby147
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(Original post by white_o)
Thank you so much! So in cardiac muscle it's only via Ryanodine receptors, not IP3, and in vascular smooth muscle it's only via IP3 but not Ryanodine receptors?
Almost.For cardiac muscle yes it’s only via Ryanodine receptors on SR ,for vascular it can be via IP3 receptors or ryanodine receptors.
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bobby147
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(Original post by white_o)
Thank you so much! So in cardiac muscle it's only via Ryanodine receptors, not IP3, and in vascular smooth muscle it's only via IP3 but not Ryanodine receptors?
Hope it helps you by seeing this overview diagram of the contractile mechanism.As you can see, the are more ways to release calcium intracellularly with vascular smooth cells compared to cardiac.

Vascular still use ryanodine receptors but it’s not necessary.As you can imagine ,if you released enough calcium via Gq,you can get smooth muscular contraction without necessarily needing to open ryanodine receptors .
Think of it as vascular can get increase in calcium
via either ryanodine or IP3, or likely sometimes using both.

Hope this helps.
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