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The muscarinic acetylcholine receptor in the heart is primarily the M2 subtype, a G protein-coupled receptor (GPCR) that mediates parasympathetic nervous system effects on cardiac tissue. Activation of cardiac M2 receptors by acetylcholine results in slowing heart rate, decreasing AV conduction, and reducing atrial contractility. This is achieved through Gi/o coupling, which inhibits adenylate cyclase and activates inward rectifier K+ channels. Drugs targeting this pathway are used clinically for arrhythmias or bradycardia management. Alterations or dysfunctions can contribute to arrhythmias or abnormal autonomic regulation.
Gi/o protein activation, inhibition of adenylate cyclase, decreased cAMP levels, activation of inward rectifier K+ channels (I_{K,ACh})
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