The SA node pacemaker potential !
- Mechanism
- Exam priority: high
Cells in the sinus node slowly charge themselves up until they fire, which sets the heart rate without any nerve signal.
Updated 2026-11-01
Also called: Slow-response action potential, Funny current (If)
See it in 3D: Sinoatrial (SA) node · Right atrium · Vagus nerve
What it is
Sinoatrial (SA) node cells have no stable resting potential. During diastole they depolarize slowly (phase 4) until they reach threshold and fire a Ca²⁺-driven action potential. Because they reach threshold first, they set the rate of the whole heart; autonomic nerves change the rate by changing the slope of phase 4.
How it works, step by step
- After repolarization the cell reaches its most negative value, about −60 mV.
- Hyperpolarization opens HCN channels; Na⁺ leaks in (funny current) and the membrane drifts upward.
- Near −50 mV T-type Ca²⁺ channels add inward current and K⁺ outflow keeps falling.
- At ≈ −40 mV L-type Ca²⁺ channels open and the cell fires a slow upstroke.
- K⁺ channels then repolarize the cell and the cycle begins again.
- Noradrenaline on β1 receptors raises cAMP, which increases If and Ca²⁺ currents: phase 4 is steeper and threshold is reached sooner.
- Acetylcholine on M2 receptors lowers cAMP and opens K⁺ channels: the cell starts more negative, the slope flattens and rate falls.
Action potential
Maximum diastolic potential −60 mVThreshold −40 mVPeak +10 mVCycle ≈ 700 ms (≈ 85 bpm)
Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.
- Mainly Na⁺
- Mainly K⁺
- Mainly Ca²⁺
- Maximum diastolic potential
- Threshold
- ARP: absolute refractory period
- RRP: relative refractory period
Reference values
| Parameter | Value |
|---|---|
| Maximum diastolic potential (SA node) | ≈ −55 to −60 mV |
| Threshold (SA node) | ≈ −40 mV |
| Intrinsic SA rate (denervated heart) | ≈ 100/min |
| Resting adult heart rate | 60–100/min |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Sympathetic nerves and adrenaline (β1): Steeper phase 4, faster heart rate (positive chronotropy).
- −Vagus nerve (ACh on M2): Hyperpolarizes the cell and flattens phase 4: slower heart rate.
- +Fever, hyperthyroidism: Faster spontaneous depolarization and higher rate.
- −Beta blockers, hypothermia: Less steep phase 4 and slower rate.
Clinical notes
- Sick sinus syndrome (and Chagas cardiomyopathy, common in Colombia) can damage the SA node, giving bradycardia and escape rhythms from lower pacemakers.
- A well-trained athlete has high vagal tone and may have a resting rate below 50/min without disease.
Test yourself
Think of the answer, then tap the question to see it.
Why is the upstroke of an SA node action potential slow compared with a ventricular myocyte?
It is carried by L-type Ca²⁺ channels, which open and pass current more slowly than the fast Na⁺ channels; at nodal potentials most Na⁺ channels are inactivated.
How does vagal stimulation lower heart rate at the level of the SA node cell?
ACh on M2 receptors opens K⁺ channels (hyperpolarizing the cell) and lowers cAMP (less funny current), so phase 4 starts lower and rises more slowly.
If the SA node fails, what rhythm and rate would you expect next?
An escape rhythm from the AV junction at about 40–60/min; if that also fails, a ventricular escape at about 20–40/min with wide QRS complexes.
A heart transplant recipient has a resting rate near 100/min. Why?
The transplanted heart is denervated, so there is no vagal tone; the SA node beats at its intrinsic rate, which is faster than the usual resting rate.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The ventricular action potential
- The cardiac conduction system
- How arrhythmias arise
- Nervous control of the circulation and the CNS ischemic response
Related conditions
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 19.2 Cardiac Muscle and Electrical Activity (OpenStax (Rice University), 2022); 19.4 Cardiac Physiology (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 10). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.