## Parasympathetic Neurotransmission at the Sinoatrial Node **Key Point:** Acetylcholine (ACh) is the universal neurotransmitter released by all postganglionic parasympathetic nerve terminals, including those innervating the sinoatrial (SA) node. ### Mechanism of Action Postganglionic parasympathetic neurons release acetylcholine, which binds to **M2 muscarinic receptors** on SA nodal pacemaker cells. This activation: - Increases K⁺ conductance (hyperpolarization) - Decreases cAMP levels - Reduces L-type Ca²⁺ channel activity - **Result:** Decreased heart rate (negative chronotropic effect) ### Autonomic Neurotransmitter Distribution | Location | Parasympathetic | Sympathetic | |----------|-----------------|-------------| | SA node | ACh (M2) | Noradrenaline (β1) | | AV node | ACh (M2) | Noradrenaline (β1) | | Atrial muscle | ACh (M2) | Noradrenaline (β1) | | Ventricular muscle | ACh (minimal) | Noradrenaline (β1) | **High-Yield:** All postganglionic parasympathetic terminals use acetylcholine as their neurotransmitter, regardless of target organ (heart, GI tract, eye, bladder). This is a fundamental principle of autonomic physiology. **Clinical Pearl:** Vagal stimulation (parasympathetic) → ACh release → M2 receptor activation → bradycardia and AV nodal delay. This is why vagal maneuvers and adenosine (which mimics vagal effects) slow AV conduction.
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