Cardiac Myocyte Action Potential
Overview: Cardiac myocytes have a unique action potential characterized by a prolonged plateau phase, which is essential for effective contraction of the heart. The ventricular action potential lasts approximately 200–400 ms.
Phases of Cardiac Myocyte Action Potential:
Phase 0 – Rapid Depolarization:
– Event: Fast upstroke of the action potential.
– Ion channels: Voltage-gated Na+ channels open.
– Ion movement: Na+ flows into the cell.
– Membrane potential: Rises from ~-90 mV to about +20 mV.
– Significance: Initiates contraction.
Phase 1 – Initial Repolarization:
– Event: Slight repolarization after the peak.
– Ion channels: Transient K+ channels (Ito) open briefly.
– Ion movement: K+ flows out of the cell.
– Membrane potential: Drops slightly from +20 mV to around 0 mV.
– Significance: Prepares for plateau phase.
Phase 2 – Plateau:
– Event: Prolonged depolarization.
– Ion channels: L-type Ca2+ channels open; some K+ channels remain open.
– Ion movement: Ca2+ in, K+ out.
– Membrane potential: Remains around 0 mV for ~200 ms.
– Significance: Sustains contraction and triggers calcium-induced calcium release.
Phase 3 – Rapid Repolarization:
– Event: Membrane potential returns to resting.
– Ion channels: L-type Ca2+ channels close; delayed rectifier K+ channels open fully.
– Ion movement: K+ flows out.
– Membrane potential: Returns to ~-90 mV.
– Significance: Ends contraction and prepares cell for next action potential.
Phase 4 – Resting Membrane Potential:
– Event: Cell is at rest.
– Ion channels: Inward rectifier K+ channels (IK1) maintain resting potential; Na+/K+ ATPase maintains gradients.
– Membrane potential: ~-90 mV.
– Significance: Stable resting state, ready for next action potential.
Key Features:
– Long-duration action potential prevents tetany.
– Calcium influx during plateau is crucial for excitation–contraction coupling.
– Effective refractory period lasts nearly the entire action potential, preventing premature re-excitation.
Diagram of Cardiac Action Potential:
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