The Effects of Second Messengers on Muscle

See my previous article about muscle contraction here.


Second messengers such as cAMP and Ca2+ help transmit and amplify cellular signals. Various muscle types respond to these messengers in different ways.

I’m skeptical about the alpha-1 receptors — here, it says they promote pupil dilation. However, in the previous image, it says that alpha-1s promote smooth muscle contraction which logically leads to pupillary constriction. But then all sympathetic responses involving adrenergic receptors should involve dilation! I think the discrepancy comes from the fact that some muscles need to contract and some need to relax to facilitate pupil dilation. Science is so wonderfully confusing LOL

Also please excuse the terrible pic quality - I pulled this second image from the depths of my camera roll and it appears that, back then, I was too lazy to screenshot and send it to my phone. But at least it’s still readable.

Ca2+ is needed for smooth muscle contraction, due to the Ca2+/calmodulin system. Thus, α1 adrenergic receptors resulting in Ca2+ release would cause smooth muscle contraction. α2 receptors inhibit Ca2+ release, thereby inhibiting neurotransmitter release. Ca2+ is necessary for vesicular mobilization to allow for release of their contents. This process is mediated by SNARE proteins. Additionally, in any Ca2+ associated pathway, PKC (a serine/threonine kinase) will be involved in phosphorylating the necessary residues to activate proteins.

The α2 receptor also causes inhibition of cAMP via the Gi pathway. cAMP allows dephosphorylation of myosin light chain kinase (MLCK), which causes smooth muscle relaxation. Thus, a reduction in cAMP would cause smooth muscle contraction. Also, cAMP decreases [Ca2+] which may contribute to smooth muscle relaxation.

Interesting quirk: notice how dephosphorylated MLCK is inactive, instead of phosphorylated being active.

β receptor activation causes cAMP formation through the Gs pathway. By the opposite process of that outlined above, smooth muscle relaxes. More cAMP causes heart muscle contraction, as cAMP activates PKA (a serine/threonine kinase), which phosphorylates the L-type Ca2+ channel and Ryanodine receptor, freeing more Ca2+ for contraction. Additionally, cAMP encourages glycogenolysis via activating PKA, which activates glycogen phosphorylase, allowing glycogenolysis in response to E and NE.

Here are some resources I found helpful:

PS - IT’S TIME FOR A RANDOM NOTE!

epinephrine response

  • liver: beta adrenergic receptors, cAMP→PKA→glycogen phosphorylase to break glycogen

  • smooth muscles of blood vessels: relax due to beta adrenergic activation, increased blood flow

  • intestines: alpha adrenergic, Gi, decreased blood flow to the area too

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Where to? — How Newly-Translated Proteins Find Their New Cellular Homes

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