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During Parasympathetic action when acetlcholine is released in the sphincter muscles then the M3 muscarinic receptors stimulate Gq protein and this in turn activate Phospholipase C (PLC). PLC then cleaves the phospholipid. In the process, phosphatidylinositol 4,5-bisphosphate (PIP2) is cleaved into diacyl glycerol (DAG) and inositol 1,4,5-triphosphate (IP3). DAG remains bound to the membrane and IP3 is released as a soluble structure in the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly the calcium channels in the endoplasmic reticulum (ER). These channels are specific to calcium and allow only the passage of calcium to move through. This causes the cytosolic concentration of calcium to increase and cause the cascade of contractile machinery and the spinchter will contract and tighten up.

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How would a drug that blocks acetylcholine release affect muscle contraction?

All I know is that acetylcholine is the only neurotransmitter that transmits signals from nerves to skeletal muscles, so anything that blocks it would probably have the effect of you wanting to move your muscles, but either not being able to, or moving weakly. Just a (educated) guess. It would cause spastic paralysis (muscles are contracted and unable to relax)


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If the enzyme that breaks down acetylcholine is destroyed, acetylcholine levels in the body will increase. This can lead to overstimulation of muscles and nerves, causing symptoms like muscle twitching, paralysis, respiratory failure, and even death.


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