GI System MCAT Practice Question
A 58-year-old man presents with chronic epigastric pain and early satiety. Upper endoscopy reveals chronic gastritis with reduced gastric acid production. A research team investigates the patient's gastric physiology by studying chief cell function in vitro. When isolated chief cells from a control subject are exposed to acetylcholine, pepsinogen secretion increases significantly. However, when chief cells are pre-treated with atropine (a muscarinic receptor antagonist), the acetylcholine-induced pepsinogen secretion is completely blocked. Atropine does not affect pepsinogen release induced by direct application of inositol 1,4,5-trisphosphate (IP3) to the cytoplasm. Which of the following best explains the mechanism by which acetylcholine stimulates pepsinogen secretion in chief cells?
Answer choices
- AAcetylcholine binds nicotinic receptors on chief cells, causing sodium influx and membrane depolarization
- BAcetylcholine activates muscarinic M3 receptors, triggering phospholipase C activation, IP3 generation, and intracellular calcium releaseCorrect answer
- CAcetylcholine inhibits phosphodiesterase activity, leading to increased intracellular cAMP and protein kinase A activation
- DAcetylcholine binds to M2 receptors, which directly inhibit adenylyl cyclase and reduce inhibitory cAMP signaling
- EAcetylcholine competitively blocks somatostatin receptors on chief cells, removing inhibition of pepsinogen release
- FAcetylcholine activates voltage-gated calcium channels directly, bypassing receptor-mediated signaling
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