Excitation-contraction Coupling Of Cardiac Cells

-94 mV


5 mM

120 mM

24 m

-83 mV


10-7 M

2 mM

2 x 104

+129 mV

Eion, the equilibrium potential calculated from the Nernst equation.

Eion, the equilibrium potential calculated from the Nernst equation.

Equilibrium Potential For SodiumSinoatrial Node Cell

Sinoatrial node 150 ms

Action Potential Duration Atrium 150 ms

Ventricle 250 ms

Purkinje fibers 300 ms

Fig. 14. Ionic conductance changes during the ventricular cardiac action potential. See text for details.

4.1 Cardiac Action Potentials

Cardiac action potentials occur because of transient changes in the cellular permeability to sodium, calcium, and potassium. A brief increase in sodium permeability depolarizes the cell and drives the membrane potential toward the sodium equilibrium potential (Fig. 14). This activates voltage-gated calcium and potassium channels. The subsequent opening of calcium channels allows calcium to enter the myocyte and sustains the depolarized state. The opening of the potassium channels allows potassium efflux from the cell and thus drives the membrane potential back toward the potassium equilibrium potential (more negative). The timing of these changes depends on the isoforms of the channel proteins present in each cell, with sinoatrial and atrial muscle action potentials lasting about 150 ms, ventricular muscle about 250 ms, and Purkinje fibers about 300 ms (see also Chapter 9). The primary difference between these cell types is often the duration of the plateau phase (phase 2), which is primarily a response to calcium channels (Fig. 15).

Fast-response cardiac cells, such as those of atrial and ventricular muscle and the Purkinje fibers, have an extremely rapid phase 0 or transition from the resting membrane potential to depolarization. As the sodium channels begin to close, an initial repolarization occurs that is labeled phase 1 . The opening of the L-type calcium channels and voltage-gated potassium channels results in a calcium influx that balances the potassium efflux. This results in the positive plateau (phase 2) of the fast-response action potential profile. As the calcium channels close, the potassium channels begin to dominate, and full repolarization of the cells occurs. From the initiation of the action potential through approximately half of the repolarization, the cell is refractory, meaning that it cannot respond to a new depolarization signal.

4.2. Pacemaker Cells

Slow-response cardiac cells, like sinoatrial and atrioven-tricular nodal cells, have what are considered unstable resting potentials; a gradual rise in their resting potentials crosses the threshold for opening of T-type calcium channels. The movement of calcium into the cells (phase 0) initiates depolarization. No initial repolarization or plateau occurs, so phases 1 and 2 are said to be absent. Repolarization (phase 3) is accomplished through the opening of voltage-gated potassium channels. Once the cell is repolarized (phase 4), leak channels (often attributed to slow sodium channels) contribute to instability of the resting potential and a gradual rise to the threshold value of the T-type calcium channels (Fig. 15).

The sinoatrial node is a specialized collection of cardiac myocytes in the right atrium that acts as the intrinsic cardiac pacemaker. The unstable resting potentials of the sinoatrial nodal cells lead to spontaneous depolarizations with a relatively rapid and regular repeat (i.e., more rapid than all other myocytes). The rapid pace of the depolarizations of the sino-atrial node contol cardiac activation through the principle of overdrive suppression. This principle states that the myocytes with the most rapid frequency of depolarization control the overall rhythm of the heart.The action potential of the sinoatrial node is sometimes referred to as a "slow response" because the upstroke of the depolarization is slower than that of the nonnodal cardiac cells that provide the contractile force during atrial or ventricular contraction. However, the rapid repeat of this depolarization gives the sinoatrial node overall control of the heart rate. The atrioventricular node works similarly but has a slower rate and is normally under the control of the sinoatrial node. In the event of damage to the sinoatrial node, the atrioventricular node assures ventricular contractions at its native (slower) rate. For additional details on cardiac action potential, see Chapter 9.

Excitation-contraction-coupling in cardiac muscle can be considered to begin with the depolarization of the sinoatrial node; this excitation quickly passes via gap junctions from cell to cell (Fig. 16). In contractile cardiac myocytes, this depolarization opens the voltage-gated sodium channels, which ultimately triggers the opening of the voltage-gated calcium channels. The opening of these channels results in increases of the myoplasmic calcium concentration, which in turn triggers calcium release from the sarcoplasmic reticulum; this last process is called calcium-induced calcium release. As noted in Section 2.2, the calcium binds to TnC on the thin filaments, causing conformational changes of this protein and then inducing the movement of Tm away from the myosin-binding site on actin. Myosin is then free to bind to actin and generate force.

Relaxation requires reduction of the internal calcium concentration. ATP-dependent calcium pumps in the sarcoplas-mic reticulum resequester calcium into the lumen of this vesicular system. In myocytes, calcium pumps in the plasma membrane also help reduce cytosolic calcium by pumping calcium into the extracellular space. Furthermore, the sodium-calcium exchanger moves one calcium ion out of the cell at the expense of bringing in three sodium ions. The balance of sodium and potassium is restored through the action of the ATP-dependent Na/K-ATPase (adenosine triphosphatase). The use of these ion motive pumps reveals an important energetic consideration: For cardiac myocytes, both the contraction and relaxation of the cells require ATP.

Relative Refractory Period
Fig. 15. Phases of the cardiac action potential. Phase 0, upstroke; phase 1, initial repolarization; phase 2, plateau; phase 3, repolarization; phase 4, resting membrane potential. ERP, effective refractory period; RRP, relative refractory period. See text for further details.
Relative Refractory Period
Fig. 16. Excitation-contraction-coupling in cardiac myocytes. The cascade of events that follow a cardiac action potential resulting in cellular contraction followed by relaxation. See text for details.

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