In Chapters 6 and 7, we discussed the ionic mechanisms underlying the action potential of nerve membrane. The action potential of skeletal muscle fibers is fundamentally the same as that of neurons. The cardiac action potential, however, is different from these other action potentials in several important ways. Figure 12-5 compares the characteristics of action potentials of skeletal and cardiac muscle cells. One striking difference is the difference in time-scale: cardiac action potentials can last several hundred milliseconds, while skeletal muscle action potentials are typically over in 1-2 msec. As we saw in Chapter 6, a long-lasting plateau like that of the cardiac action potential can arise from a calcium component in the action potential, resulting from the opening of voltage-dependent calcium channels. These channels open upon depolarization and allow influx of positively charged calcium ions. In addition, the plateau of the cardiac action potential is also associated with a reduction in the potassium permeability. This is due to a type of potassium channel that is open as long as the membrane potential is near its normal resting level and closes upon depolarization. This is the reverse of the behavior of the gated potassium channel we are familiar with from our discussion of nerve action potential. The reduction in potassium permeability caused by the closing of this channel
tends to depolarize the cardiac muscle fiber. Both the opening of the calcium channels and the closing of the potassium channels contribute to the plateau.
The initial rising phase ofthe cardiac action potential is produced by voltage-dependent sodium channels very much like those of nerve membrane. The sodium channels drive the rapid initial depolarization and are responsible for the brief initial spike of the cardiac action potential before the plateau phase sets in. Like the sodium channel of neuronal membrane, this channel rapidly closes (inactivates) with maintained depolarization. However, unlike the nerve sodium channel, this inactivation is not total; there is a small, maintained increase in sodium permeability during the plateau.
What is responsible for terminating the cardiac action potential? First, the calcium permeability of the plasma membrane slowly declines during the maintained depolarization. This decline might be a consequence of the gradual build-up of internal calcium concentration as calcium ions continue to enter the muscle fiber through the open calcium channels. Internal calcium ions are thought to have a direct or indirect action on the calcium channels, causing them to close. In addition, the potassium permeability of the plasma membrane increases, as in the nerve and skeletal muscle action potentials. This increase in potassium permeability tends to drive the membrane potential of the cardiac fiber toward the potassium equilibrium potential and thus to repolarize the fiber. There is evidence that part of this increase in potassium permeability is due to voltage-sensitive potassium channels that open in response to the depolarization during the action potential (like the n gates of the nerve membrane). However, the increased potassium permeability is also caused by calcium-activated potassium channels (see Chapter 6), which open in response to the rise in internal calcium concentration during the prolonged action potential.
One functional implication of the prolonged cardiac action potential is that the duration of the contraction in cardiac muscle is controlled by the duration of the action potential. The action potential and contraction of cardiac muscle fibers are compared with those of skeletal muscle fibers in Figure 12-6. In skeletal muscle, the action potential acts only as a trigger for the contractile events; the duration of the contraction is controlled by the timing of the release and
Figure 12-6 (a) In a skeletal muscle fiber, the action potential is much briefer than the resulting contraction. Thus, the action potential acts only as a trigger for the contraction, which proceeds independently of the duration of the action potential. (b) In a cardiac muscle fiber, the duration of the contraction is closely related to the duration of the action potential because of the maintained calcium influx during the plateau of the action potential. Thus, characteristics of the action potential can influence the duration and strength of the cardiac contraction.
reuptake of calcium by the sarcoplasmic reticulum, not by the duration of the action potential. In cardiac muscle fibers, however, only the initial part of the contraction is controlled by sarcoplasmic reticulum calcium; the contraction is maintained by the influx of calcium ions across the plasma membrane during the plateau phase ofthe cardiac action potential. For this reason, the duration of the contraction in the heart can be altered by changing the duration of the action potential in the cardiac muscle fibers. This provides an important mechanism by which the pumping action of the heart can be modulated.
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