Learning Objective
After completing this section, learners will be able to describe the phases of the nodal action potential, explain the ionic currents responsible for pacemaker activity, and understand the pharmacological modulation of SA and AV node conduction.
Nodal tissue, including the SA node and AV node, lacks fast voltage-gated sodium channels. Therefore, the upstroke of the action potential is mediated primarily by calcium influx, rather than sodium. Phases 1 and 2, seen in ventricular myocytes, are absent in nodal tissue.
Phase 4 – Pacemaker (Spontaneous Depolarization)
Nodal cells show automaticity, meaning they spontaneously depolarize at rest. This pacemaker potential is generated by:
Inward Ca²⁺ current (T-type Ca²⁺ channels)
- Open at negative potentials (~ –70 mV)
- Contribute to early depolarization
Inward Na⁺ current (“Funny current,” If)
- Mediated by HCN channels (hyperpolarization-activated cyclic nucleotide-gated)
- Channels open when the membrane is negative and close during depolarization
- Conduct both Na⁺ and K⁺; depolarization is mainly due to Na⁺ entry
Reduced outward K⁺ current
- K⁺ efflux is lower during repolarization
- Helps drive the membrane potential toward threshold
Phase 0 – Upstroke of Action Potential
- Mediated primarily by L-type Ca²⁺ channels
- Slope is gradual, not steep like Na⁺-dependent upstroke in ventricular myocytes
- Results in slow conduction velocity, especially through the AV node
Phase 3 – Repolarization
- Voltage-gated K⁺ channels open
- K⁺ exits the cell → membrane repolarizes
