Compared with the action potential of a ventricular myocyte, the sinoatrial node action potential has a slow rate of rise in phase 0. The reason is that the SA node action potential upstroke depends mainly on:

• A Fast voltage-gated sodium channels with a high density of inward current
• B Chloride influx through ligand-gated channels
• C Inward rectifier potassium channels closing slowly
• D L-type voltage-gated calcium channels opening near a threshold of about minus 40 mV ✓

Explanation

SA node cells have essentially no functional fast sodium channels because their maximum diastolic potential of about minus 60 mV inactivates them. Phase 0 therefore relies on L-type calcium channels activated around minus 40 mV, producing a slow upstroke and slow conduction. Fast sodium channels dominate the steep phase 0 of ventricular muscle, which is exactly the feature described in option A, and potassium channel closure shapes repolarisation and pacemaker behaviour rather than generating the upstroke.

Reference: Ganong Review of Medical Physiology, 26th ed.

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