Diad

Myocytes are incredibly specialized cells with only a select number of different organelle types. A myocyte is composed of multiple myofibrils, which contain the “contractile units” of the muscle known as a sarcomere.^[3] These sarcomeres are arranged in adjacent formations along the myofibrils. Similarly to the plasma membrane of other cells, the sarcolemma protects and surrounds the myocytes. The two cellular components that perform the “sliding filament” contraction are myosin and actin, also referred to as the thick and thin filaments respectively^[2] The striations viewed using microscopy of the cardiac muscle are a result of the contrast between the thick and thin filaments. The z-line defines the borders of each sarcomere and act as the connection point between the thin filaments. The t-tubules and sarcoplasmic reticulum are used in conjunction to receive and direct the calcium ions and cause contraction. Once contracted, the clear H-zone between the actin filaments disappears as the filaments move towards each other.

Cardiomyocytes are a particular form of myocyte, only present in heart tissue. Along with the basic myocyte elements, these cells also contain one to four nuclei and a large amount of

Within the sarcolemma of the myocyte, there are specific invaginations referred to as transverse- tubules. These structures attached to the sarcomere z-lines help to promote interaction between the extracellular space and the interior of the cell.^[1] Connecting these tubules to the Z line allows for a closer range of excitation- contraction coupling within the cell.^[1] Within the t-tubules, distinct ion channels and cellular proteins are present within the t- tubule bilayer that allow movement of calcium influx from the extracellular space into the myocyte to initiate depolarization and contraction. Once traveling through the t- tubules, the calcium arrives at the sarcoplasmic reticulum.

Sarcoplasmic Reticulum

Within the lumen of the cardiac myocyte, the sarcoplasmic reticulum serves as the area of controlling the amount of calcium influx into the interior of the cell.

The tension felt in muscles from prolonged contraction can be attributed to extended release of calcium ions through the sarcoplasmic reticulum. By absorbing calcium ions after contraction, the sarcoplasmic reticulum can regulate muscle fatigue and prevent overuse damage within the body.

Voltage-Gated Calcium Channels

Voltage- gated calcium channels play a critical role in controlling the influx of calcium ions into the myocyte in response to the changing action potential of the sarcoplasmic membrane.^[5] The increase in action potential of the cell indicates depolarization of the cell, directly opening the ion channels to cause muscular contraction. When the action potential decreases, the ion channels close, preventing any calcium influx and further muscular contraction. This fluctuation within the myocyte contributes to the rhythmic “pacemaking” of the cardiac tissue.

There are two classes of voltage- gated calcium channels, L- type and T- type.^[5] L-type calcium channels are more commonly found in myocardial tissue throughout the heart whereas T-type calcium channels are more concentrated in the pacemaker cells of the sinoatrial node. These channels also have slightly different activation levels. The L- type responds to a more positive action potential while the T- type channels are triggered at a more negative action potential. Discrepancies and/ or malfunctioning of these gates can contribute to a number of cardiac conditions, such as bradycardia.

Cardiac Conditions Due to Diad Defects

Because the structural organization of the myocyte is very complex and specific, changes to their arrangement and/ or function can cause cardiac illnesses or defects. For example, a leading cause of heart failure can be attributed to the lack of t- tubule and sarcoplasmic reticulum junctions or a decreased distance between the structures.^[6] This change in structure causes the excitation- coupling response in the myocyte to either lessen significantly or be completely diminished. Therefore, few to no heart contractions would take place causing heart failure. On the contrary, an increase in the distance of the junction can create an increased excitation- coupling response, shown in both hypertension and cardiomyopathy.^[6] These conditions are proof that even the smallest changes in a complex structure can have long- range consequences.

References

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