A cardiac muscle action potential and isometric twitch. Because of the duration of the action potential, an effective tetanic contraction cannot be produced, although a partial contraction can be elicited late in the twitch. ARP, absolute refractory period; RRP, relative refractory period; SNP, period of supranormal excitability.
ization is from additional SR just inside the cell membrane. As in skeletal muscle, the principal role of the SR is in the rapid release, active uptake, storage, and buffering of cy-tosolic calcium. The action of calcium ions on the tro-ponin-tropomyosin complex of the thin filaments is similar to that in skeletal muscle, but cardiac muscle differs in its cellular handling of the activator, calcium.
Along with the calcium ions released from the SR, a significant amount of calcium enters the cell from outside during the upstroke and plateau phase of the action potential (see Fig. 10.2). The principal cause of the sustained depolarization of the plateau phase is the presence of a population of voltage-gated membrane channels permeable to calcium ions. These channels open relatively slowly; while open, there is a net influx of calcium ions, called the slow inward current, moving down an electrochemical gradient. Although the calcium entering during an action potential does not directly affect that specific contraction, it can affect the next contraction, and it does increase the cellular calcium content over time because of the repeated nature of the cardiac muscle contraction.
In addition, even a small amount of Ca2 + entering through the sarcolemma causes the release of significant additional Ca2+ from the SR, a phenomenon known as calcium-induced calcium release (similar to that in smooth muscle). This constant influx of calcium requires that there be a cellular system that can rid the cell of excess calcium. Regulation of cellular calcium content has important consequences for cardiac muscle function, because of the close relationship between calcium and contractile activity.
during this period, the action potentials that are produced have reduced amplitude and duration and give rise to only small contractions. This period of supranormal excitability can lead to unwanted and untimely propagation of action potentials that can seriously interfere with the normal rhythm of the heart.
The long-lasting refractoriness of the cell membrane effectively prevents the development of a tetanic contraction (see Fig. 10.2); any failure of cardiac muscle to relax fully after every stimulus would make it quite unsuitable to function as a pump. When cardiac muscle is stimulated to contract more frequently (equivalent to an increase in the heart rate), the durations of the action potential and the contraction become less, and consecutive twitches remain separate contraction-and-relaxation events.
It must be emphasized that contraction in cardiac muscle is not the result of stimulation by motor nerves. Cells in some critical areas of the heart generate automatic and rhythmic action potentials that are conducted throughout the bulk of the tissue. These specialized cells are called pacemaker cells (see Chapter 13).
The rapid depolarization associated with the upstroke of the action potential is conducted down the T tubule system of the ventricular myocardium, where it causes the release of intracellular calcium ions from the SR. In cardiac muscle, a large part of the calcium released during rapid depolar-
Was this article helpful?