Myocardial stimulators: function of calcium ions and transverse tubules

2021-06-03 04:19 PM

The contractility of the myocardium depends greatly on the concentration of calcium ions in the extracellular fluid, a heart placed in a calcium-free solution will quickly stop beating.

The term "stimulation-contraction pair" refers to the mechanism by which an action potential causes the myofibrils in the muscle to contract. Again, there are differences in this mechanism in the myocardium that have an important influence on the contractility of the myocardium.

Like skeletal muscle, when an action potential crosses the myocardium, the action potential spreads within the myocardium along the membrane of the transverse tubes (T). The action potentials in the T-tubules propagate to the membranes of the longitudinal tubules of the sarcoma, releasing calcium ions into the muscle from the endoplasmic reticulum. For another few 1/1000 s, these calcium ions diffuse into the myofibrils and catalyse chemical reactions that catalyse the sliding of the actin and myosin filaments along the myofibril, causing the muscle to contract.

Thus, this mechanism of the excitatory-contractile pair is the same as that of skeletal muscle, but with a rather different effect. Furthermore, for calcium ions to be released into the muscle from the endoplasmic reticulum vesicles, calcium ions also diffuse into the plasma on their own from the T-tubule during the action potential, when the calcium channel is potentiated. opens in the membrane of the T-tubule. Calcium enters the cell and then activates the calcium-releasing channel, also known as the ryanodine receptor channel, in the membrane of the endoplasmic reticulum, releasing calcium into the plasma. The calcium ions in the plasma then interact with troponin to initiate bridge formation and contraction.

Without calcium from the T-tubules, myocardial contractility would be greatly reduced because the endoplasmic reticulum of the myocardium is much less developed than in skeletal muscle and does not store calcium to supply full contraction. muscle. However, the T-tubes of the myocardium is 5 times the circumference of the tubules of the striated muscle, which means that the volume will be 25 times larger. In addition, the inner surface of the T-tubule has a large amount of negatively charged mucopolysaccharides and captures an abundant reserve of calcium ions, ready to diffuse into the myocardium when a T-tube action potential appears.

The contractility of the myocardium depends greatly on the concentration of calcium ions in the extracellular fluid. In fact, a heart placed in a calcium-free solution will quickly stop beating. The reason is that the opening of the T-tubule opens directly across the myocardial cell membrane to enter the intercellular space, allowing the extracellular fluid in the myocardial interstitial to permeate the T-tubule. Therefore, the amount of calcium ions in the T-tubule system (ions) calcium available for myocardial contractility) depends largely on the calcium ion concentration in the extracellular fluid.

In contrast, skeletal muscle contractility is largely unaffected by moderate changes in extracellular fluid calcium concentration because skeletal muscle contractility is induced almost entirely by calcium ions released from the plasma endoplasmic reticulum. inside striated muscle fibres.

At the end of the cardiac action potential plateau phase, the influx of calcium into the muscle fibre abruptly ceases, and the calcium ions in the muscle are rapidly pumped out of the muscle fibre into the endoplasmic reticulum and extracellular fluid space. in the T-tubule. The transport of calcium back to the endoplasmic reticulum is assisted by a calcium-adenosine phosphate (ATPase) pump. Calcium ions are also pushed out of the cell by sodium-calcium counter-transport. Sodium entering the cell in this reverse transport is then pushed out of the cell by the sodium-potassium ATPase pump. As a result, contraction stops until a new action potential appears.

Contraction time

The heart muscle begins to contract a few milliseconds after the action potential begins and continues to contract up to a few milliseconds after the action potential ends. Therefore, the duration of myocardial contractility is largely the duration of the action potential, including a plateau of about 0.2 s of atrial muscle and 0.3 s of ventricular muscle.

Figure. Mechanisms of excitation-contraction and relaxation coupling in the myocardium. ATP, adenosine triphosphate.