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Muscarinic acetylcholine receptors (M2 and M3 subtypes, primarily) located on gastric smooth muscle mediate the effects of cholinergic neuron stimulation on gastric motility. Activation of these postganglionic receptors by acetylcholine (ACh), released from enteric or vagal cholinergic neurons, induces smooth muscle contraction via G protein-coupled mechanisms, enhancing gastric tone and peristalsis. Agents that stimulate cholinergic pathways (by acting as agonists or increasing ACh levels) can serve as prokinetic drugs to enhance gastric motility, while antagonists (e.g., atropine) reverse this effect[1][3][5][7].
Agonist-mediated stimulation of muscarinic receptors increases acetylcholine-driven contraction of GI smooth muscle, enhancing motility[1][3][5]. Acetylcholinesterase inhibition increases synaptic acetylcholine, indirectly stimulating muscarinic receptors. Antagonists (e.g., atropine) inhibit this pathway, reducing motility[1][3].
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