A patient with organophosphate poisoning is treated with atropine. The mechanism by which atropine reverses bradycardia in this setting specifically involves blockade of which receptor subtype at the sinoatrial node?

• A M1 muscarinic receptor (Gq-coupled, IP3/DAG pathway)
• B M3 muscarinic receptor (Gq-coupled, vascular smooth muscle)
• C Nicotinic NM receptor at the autonomic ganglion
• D M2 muscarinic receptor (Gi-coupled, decreased cAMP and activated IKACh) ✓

Explanation

The sinoatrial node expresses predominantly M2 muscarinic receptors, which are Gi-coupled. Activation by excess acetylcholine (in organophosphate toxicity) decreases cAMP and activates the inward-rectifier potassium channel (IKACh), hyperpolarising the cell and slowing spontaneous depolarisation. Atropine competitively blocks M2 receptors, reversing this bradycardia. M1 receptors mediate gland secretion and CNS effects; M3 receptors mediate smooth-muscle contraction; nicotinic NM receptors at the neuromuscular junction are not atropine's primary target for cardiac effects.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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