Action Potential Steps


meable only to K+ (potassium equilibrium potential). In contrast, when open Na+ channels predominate (as occurs at the peak of phase 0 of the action potential), the measured potential is closer to the potential that would exist if the membrane were permeable only to Na+ (sodium equilibrium potential) (see Fig. 13.2). The opening of Ca2+ channels causes the membrane potential to be closer to the calcium equilibrium potential, which is also positive,- this occurs in phase 2. Specific changes in the number of open channels for these three cations are responsible for changes in membrane permeability and the different phases of the action potential.

The Opening and Closing of Cation Channels Causes the Ventricular Action Potential

In the normal heart, the sodium-potassium pump and calcium ion pump keep the ionic gradients constant. With constant ion gradients, the opening and closing of cation

Sodium equilibrium potential

Potassium equilibrium potential

Effect of ionic permeability on membrane potential, primarily determined by the relative permeability of the membrane to Na+, K+, and Ca2 + .

Relatively high permeability to K+ places the membrane potential close to the K+ equilibrium potential, and relatively high permeability to Na+ places it close to the Na+ equilibrium potential. The same is true for Ca2 + . An equilibrium potential is not shown for Ca2+ because, unlike Na+ and K+, it changes during the action potential. This is because cytosolic Ca2+ concentration changes approximately 5-fold during excitation. During the plateau of the action potential, the equilibrium potential for Ca2 + is approximately +90 mV. Membrane permeability to Na+, K+, and Ca2+ depends on ion channel proteins (see Table 13.1).

channels and the resulting changes in membrane permeability determine the membrane potential. Figures 13.3 and 13.4 depict the membrane changes that occur during an action potential in ventricular cells.

Depolarization Early in the Action Potential: Selective Opening of Sodium Channels. Depolarization occurs when the membrane potential moves away from the K+ equilibrium potential and toward the Na+ equilibrium potential. In ventricular cell membranes, this occurs passively at first, in response to the depolarization of adjacent membranes (discussed later). Once the ventricular cell membrane is brought to threshold, voltage-gated Na+ channels open, causing the initial rapid upswing of the action potential (phase 0). The opening of Na+ channels causes Na+ permeability to increase. As permeability to Na+ exceeds permeability to K+, the membrane potential approaches the Na+ equilibrium potential, and the inside of the cell becomes positively charged relative to the outside.

Phase 1 of the ventricular action potential is caused by a decrease in the number of open Na+ channels and the opening of a particular type of K+ channel (see Fig. 13.3 and Table 13.1). These changes tend to repolarize the membrane slightly.

Late Depolarization (Plateau): Selective Opening of Calcium Channels and Closing of Potassium Channels.

The plateau of phase 2 results from a combination of the closing of K+ channels (see Fig. 13.3 and Table 13.1) and the opening of voltage-gated Ca2+ channels. These chan-

Area of depolarization resulting from artificial stimulus or pacemaker

Area of depolarization resulting from artificial stimulus or pacemaker

Skeletal Muscle Action Potential

Events associated with the ventricular action potential. (See Table 13.1 for channel details.)

Events associated with the ventricular action potential. (See Table 13.1 for channel nels open more slowly than voltage-gated Na+ channels and do not contribute to the rapid upswing of the ventricular action potential.

Repolarization: Selective Opening of Potassium Channels.

The return of the membrane potential (phase 3, or repolarization) to the resting state is caused by the closing of Ca2+ channels and the opening of particular classes of K+ channels (see Fig. 13.3 and Table 13.1). This relative increase in permeability to K+ drives the membrane potential toward the K+ equilibrium potential.

Resting Membrane Potential: Open Potassium Channels.

The resting (diastolic) membrane potential (phase 4) of ventricular cells is maintained primarily by K+ channels that are open at highly negative membrane potentials. They are called inward rectifying K+ channels because, when the membrane is depolarized (e.g., by the opening of voltage-gated Na+ channels), they do not permit outward movement of K+. Other specialized K+ channels help stabilize the resting membrane potential (see Table 13.1) and, in their absence, serious disorders of cardiac electrical activity can develop.

The Opening of Na and Ca2 and the Closing of K Channels Causes the Pacemaker Potential of the SA and AV Nodes

When the electrical activity of a cell from the SA or AV node is compared with that of a ventricular muscle cell, three important differences are observed (see Fig. 13.1, Fig. 13.5): (1) the presence of a pacemaker potential, (2) the slow rise of the action potential, and (3) the lack of a well-defined plateau. The pacemaker potential results from changes in the permeability of the nodal cell membrane to all three of the major cations (see Table 13.2). First, K+ channels, primarily responsible for repolarization, begin to close. Second, there is a steady increase in the membrane

Membrane potential V-40

K+ permeability

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  • mathias
    What would an open ca2 channel do to the resting potential?
    7 years ago
    Which phase of the ventricular muscle action potential is the potassium permeability the highest?
    6 years ago

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