Which ion channel is responsible for the plateau phase (phase 2) of the ventricular action potential, and what is its physiological significance?

• A L-type (long-lasting) voltage-gated Ca²⁺ channels; Ca²⁺ influx during phase 2 triggers calcium-induced calcium release (CICR) from sarcoplasmic reticulum, linking electrical excitation to mechanical contraction ✓
• B T-type Ca²⁺ channels; they open during the plateau and regulate pace-maker activity in ventricular myocytes
• C Funny current (If) channels (HCN); they open at −60 mV maintaining the plateau against K⁺ repolarization
• D Na⁺/Ca²⁺ exchanger (NCX); it runs in reverse mode during phase 2 generating inward current to sustain the plateau

Explanation

Phase 2 (the plateau, at approximately 0 mV for ~200 ms) is sustained by L-type Ca²⁺ channel opening, which provides a slow inward Ca²⁺ current that balances K⁺ efflux through transiently inactivated delayed rectifier K⁺ channels. The physiological importance is profound: Ca²⁺ entering through L-type channels triggers ryanodine receptor 2 (RyR2) on the sarcoplasmic reticulum to release a much larger Ca²⁺ store (CICR), producing the cytosolic Ca²⁺ transient that activates troponin C and initiates contraction. L-type blockers (calcium channel blockers) reduce contractility and prolong or abolish phase 2. T-type channels (option B) are found in pacemaker cells (SA/AV node), not ventricular myocytes. The If (option C) is involved in pacemaker depolarization (phase 4), not plateau. NCX (option D) contributes marginally but is not the primary plateau sustaining mechanism.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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