Action Potential and Ion Channels

The cardiac action potential is the transient change in membrane voltage that signals a cardiac cell's electrical activity, produced by the opening and closing of ion channels selective for sodium, calcium, and potassium. The characteristic long plateau of the cardiac action potential, set by a balance of inward and outward currents, distinguishes cardiac cells from nerve and underlies the heart's prolonged refractoriness.

Definition

A cardiac action potential is a stereotyped, regenerative change in transmembrane potential, generated by the time- and voltage-dependent flow of ions through selective channels, that propagates excitation through cardiac tissue; ion channels are the membrane proteins whose gated permeability to specific ions produces these currents.

Scope

This entry covers the phases of the cardiac action potential, the principal ionic currents and channels that shape it, the concept of refractoriness, and how action-potential properties differ between cell types in the heart. It treats these as physiological topics, not as clinical guidance on arrhythmias or drug effects.

Core questions

• What are the phases of the cardiac action potential?
• Which ionic currents shape depolarization, the plateau, and repolarization?
• Why is the cardiac action potential so much longer than a nerve action potential?
• What is refractoriness and why does it matter?

Key concepts

• Resting membrane potential
• Depolarization (phase 0)
• Plateau phase
• Repolarization
• Sodium, calcium, and potassium currents
• Voltage-gated ion channels
• Absolute and relative refractory periods
• Threshold and all-or-none response

Key theories

Ionic (Hodgkin-Huxley) theory of excitability

The action potential is explained by voltage- and time-dependent changes in membrane conductance to individual ions; this quantitative framework, originally derived for nerve, provides the basis for describing cardiac action potentials as the sum of distinct ionic currents.

Mechanisms

In a working ventricular myocyte the action potential is conventionally divided into phases. Rapid depolarization (phase 0) is driven by a large, fast inward sodium current once threshold is reached. A brief early repolarization (phase 1) reflects transient outward potassium current. The plateau (phase 2), a hallmark of cardiac cells, results from a balance between sustained inward L-type calcium current and outward potassium currents, prolonging the action potential. Repolarization (phase 3) follows as potassium currents predominate and calcium current declines, returning the membrane toward its resting potential (phase 4), which is stabilized by inward-rectifier potassium current. Because sodium channels recover from inactivation only after repolarization, the cell is refractory for most of the action potential, preventing premature re-excitation and tetanus; the molecular identities and kinetics of the underlying channels determine repolarization and refractoriness.

Clinical relevance

Action-potential shape and the channels that produce it form the physiological basis for understanding repolarization abnormalities and the actions of agents that modify ionic currents. This entry describes normal cellular electrophysiology and is educational background, not a basis for individual diagnosis or treatment.

History

The conceptual foundation was the Hodgkin-Huxley description of the nerve action potential in 1952, which expressed excitation as voltage- and time-dependent ionic conductances. These principles were later applied to cardiac cells, where the long plateau and a richer set of ionic currents were characterized, and molecular cloning eventually linked specific channel proteins to each current shaping cardiac repolarization.

Key figures

• Alan Hodgkin
• Andrew Huxley
• Jeanne Nerbonne
• Robert Kass
• Denis Noble

Seminal works

• hodgkin-huxley-1952
• nerbonne-kass-2005

Frequently asked questions

Why does the cardiac action potential have a plateau?

The plateau reflects a sustained balance between inward calcium current and outward potassium currents, which prolongs depolarization far beyond a nerve action potential and contributes to the heart's long refractory period.

What does refractoriness do?

During the refractory period the cell cannot be re-excited because sodium channels have not yet recovered from inactivation, which prevents premature beats and sustained tetanic contraction of cardiac muscle.