Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential is compared with that of a ventricular muscle fiber.
the fibers of the heart's specialized conducting system, including the fibers of the sinus node. For this reason, the sinus node ordinarily controls the rate of beat of the entire heart, as discussed in detail later in this chapter. First, let us describe this automatic rhythmicity.
Mechanism of Sinus Nodal Rhythmicity. Figure 10-2 shows action potentials recorded from inside a sinus nodal fiber for three heartbeats and, by comparison, a single ventricular muscle fiber action potential. Note that the "resting membrane potential" of the sinus nodal fiber between discharges has a negativity of about -55 to -60 millivolts, in comparison with -85 to -90 millivolts for the ventricular muscle fiber. The cause of this lesser negativity is that the cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions, and positive charges of the entering sodium and calcium ions neutralize much of the intracellular negativity.
Before attempting to explain the rhythmicity of the sinus nodal fibers, first recall from the discussions of Chapters 5 and 9 that cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels. Opening of the fast sodium channels for a few 10,000ths of a second is responsible for the rapid upstroke spike of the action potential observed in ventricular muscle, because of rapid influx of positive sodium ions to the interior of the fiber. Then the "plateau" of the ventricular action potential is caused primarily by slower opening of the slow sodium-calcium channels, which lasts for about 0.3 second. Finally, opening of potassium channels allows diffusion of large amounts of positive potassium ions in the outward direction through the fiber membrane and returns the membrane potential to its resting level.
But there is a difference in the function of these channels in the sinus nodal fiber because the "resting" potential is much less negative—only -55 millivolts in the nodal fiber instead of the -90 millivolts in the ventricular muscle fiber. At this level of -55 millivolts, the fast sodium channels mainly have already become "inactivated," which means that they have become blocked. The cause of this is that any time the membrane potential remains less negative than about -55 millivolts for more than a few milliseconds, the inacti-vation gates on the inside of the cell membrane that close the fast sodium channels become closed and remain so. Therefore, only the slow sodium-calcium channels can open (i.e., can become "activated") and thereby cause the action potential. As a result, the atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. Also, after the action potential does occur, return of the potential to its negative state occurs slowly as well, rather than the abrupt return that occurs for the ventricular fiber.
Self-Excitation of Sinus Nodal Fibers. Because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as a moderate number of already open sodium channels, positive sodium ions from outside the fibers normally tend to leak to the inside. Therefore, between heartbeats, influx of positively charged sodium ions causes a slow rise in the resting membrane potential in the positive direction. Thus, as shown in Figure 10-2, the "resting" potential gradually rises between each two heartbeats. When the potential reaches a threshold voltage of
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.