Vagal Brake on the Sinoatrial Node

Autonomic Control

Vagal tone (efferent ACh release) 30%

Sympathetic tone (β1 / cAMP) 10%

SA Node Output

Heart rate

— bpm

RR interval

— ms

Max diastolic potential

−60 mV

Phase-4 slope

— mV/ms

How it works

SA node cells never rest at a fixed resting potential — after each action potential they drift up from a maximum diastolic potential (MDP) toward threshold through phase-4 (diastolic) depolarization, driven mainly by the "funny current" I_f and T-type Ca²⁺ current:

V(t) = MDP + slope · t     (diastole, t measured from the last beat)
fires when V(t) ≥ V_threshold  →  RR interval = (V_threshold − MDP) / slope
Heart rate (bpm) = 60000 / RR(ms)

The vagus nerve releases acetylcholine (ACh) onto M2 receptors, which does two things simultaneously:

opens G-protein-coupled inward-rectifier K⁺ channels (I_KACh), hyperpolarizing the MDP;
lowers cAMP, which shifts I_f activation and flattens the phase-4 slope.

Both effects lengthen the RR interval, so heart rate falls — this simulator implements them as MDP = MDP₀ − 15·vagalTone and slope = slope₀·(1 − 0.8·vagalTone), scaled by an "accentuated antagonism" term so vagal slowing is stronger on a background of sympathetic tone, exactly as observed experimentally. Sympathetic (β1/cAMP) tone does the opposite — it steepens the slope and slightly depolarizes the MDP, speeding the node up. At very high vagal tone the slope can approach zero, reproducing transient sinus arrest; sustained supramaximal vagal stimulation is followed clinically by vagal escape, a latent pacemaker resuming the rhythm.

Respiratory sinus arrhythmia (RSA) gates vagal outflow with the breathing cycle — inspiration transiently withdraws vagal tone (HR rises), expiration restores it (HR falls) — toggle it to see the RR interval oscillate at the breathing rate. Vagal burst mimics a brief strong reflex (e.g. carotid sinus / vasovagal) discharge and its recovery.

SA node pacemaker cells Vagus nerve / ACh release

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