In the cardiac action potential of ventricular myocytes, the plateau phase (phase 2) is maintained by:
- A Balance between inward L-type Ca2+ current (ICaL) and outward delayed rectifier K+ currents (IKr and IKs) ✓
- B Persistent inward Na+ current (INa) maintaining depolarisation against rapid K+ repolarisation
- C Sodium-calcium exchanger (NCX) operating in reverse mode, bringing Ca2+ in and extruding Na+
- D T-type Ca2+ channels exclusively sustaining the plateau in mid-ventricular myocytes
Explanation
The prolonged plateau (phase 2) of the ventricular action potential is unique to cardiac muscle and is responsible for the long refractory period. It results from a dynamic balance between: (1) inward Ca2+ current via long-opening L-type (dihydropyridine-receptor) calcium channels (ICaL), which maintains near-zero net charge movement, and (2) slowly activating outward K+ currents — the rapid (IKr) and slow (IKs) delayed rectifier K+ channels. This balance keeps membrane potential near 0 mV for 200–300 ms. L-type Ca2+ channels are blocked by verapamil and diltiazem. IKs is blocked by Class III antiarrhythmics. The plateau is critical for triggering calcium-induced calcium release from the SR and ensuring adequate mechanical contraction.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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