A student administers a very low dose of atropine to a volunteer and is surprised to record a slowing of heart rate rather than the expected tachycardia. The best explanation for this paradoxical bradycardia is:
- A Direct stimulation of cardiac M2 receptors by atropine at low concentrations
- B Blockade of presynaptic muscarinic autoreceptors that normally inhibit acetylcholine release from vagal terminals, increasing vagal outflow ✓
- C Reflex baroreceptor activation caused by atropine-induced vasodilation at low doses
- D Atropine enhances norepinephrine release from cardiac sympathetic nerves at low doses
Correct answer: B. Blockade of presynaptic muscarinic autoreceptors that normally inhibit acetylcholine release from vagal terminals, increasing vagal outflow
Explanation
At therapeutic doses atropine blocks postsynaptic M2 receptors on the SA node, abolishing vagal slowing and causing tachycardia. At very low doses it preferentially blocks presynaptic muscarinic autoreceptors on vagal nerve endings, which normally mediate feedback inhibition of acetylcholine release. Loss of this brake increases acetylcholine release and slows the heart. Atropine does not stimulate M2 receptors, and the effect is independent of baroreflexes.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.