 Gap junctions (communicating junctions) constitute the major structural element of the lateral component of the intercalated disc. Gap junctions provide ionic continuity between adjacent cardiac muscle cells, thus allowing informational macromolecules to pass from cell to cell. This exchange permits cardiac muscle fibers to behave as a syncytium while retaining cellular integrity and individuality. The position of the gap junctions on the lateral surfaces of the intercalated disc protects them from the forces generated during contraction.
The sER in cardiac muscle cells is organized into a single network along the sarcomere, extending from Z line to Z line.
The sER of cardiac muscle is not as well organized as that of skeletal muscle. It does not separate bundles of myofilaments into discrete myofibrils. The T tubules in cardiac muscle penetrate into the myofilament bundles at the level of the Z line, between the ends of the sER network. Thus, there is only one T tubule per sarcomere in cardiac muscle. Small terminal cisternae of the sER are in close proximity to the T tubules to form a diad at the level of the Z line (see Fig. 11.15). The external lamina adheres to the invaginated plasma membrane of the T tubule as it penetrates into the cytoplasm of the muscle cell. The T tubules are larger and more numerous in cardiac ventricular muscle than in skeletal muscle. They are less numerous, however, in cardiac atrial muscle.
Passage of Ca2 from the lumen of the T tubule to the sarcoplasm of a cardiac muscle cell is essential to initiate the contraction cycle.
As discussed in the section on skeletal muscle, depolarization of the T tubule membrane activates voltage-sensor proteins, which are similar in structure and function to Ca2 channels. In contrast to skeletal muscle, long-lasting depolarization in cardiac muscle activates these sensors and prompts their slow conformation change into functional Ca2 channels (Fig. 11.17). Thus, in the first stage of the cardiac muscle contraction cycle, Ca2 from the lumen of the T tubule is transported to the sarcoplasm of cardiac muscle, which opens gated Ca2-release channels in adjacent terminal sacs of the
FIGURE 11.17 • Movement of the calcium ions after depola rization of the plasma membrane in cardiac muscle.
Depolarization of the T tubule membrane activates voltage-sensor proteins that function as Ca2 channels. Initially, Ca2 is transported from the lumen of the T tubule through channels in voltage-sensor proteins into the sarcoplasm of the cardiac muscle (illustrated next to the upper terminal sac of the sER). Next, Ca2 activates gated Ca2-release channels in adjacent terminal sacs of the sarcoplasmic reticulum. This causes the massive release of sequestrated Ca2 from the sER into the sarcoplasm and initiates the contraction cycle.
sarcoplasmic reticulum. This calcium-triggered calcium release mechanism causes a massive and rapid release of additional Ca2 that initiates subsequent steps of the contraction cycle, which are identical to those in skeletal muscle. The differences between initiation of cardiac and skeletal muscle contractions—the longer-lasting membrane depolarization and activation of voltage-sensitive Ca2 channels in the wall of the T tubule—account for an approximately 200-millisecond delay from the start of a depolarization in a cardiac  muscle twitch (see Fig. 11.11).
Cardiac muscle cells exhibit a spontaneous rhythmic contraction.