After that, a new ATP molecule binds to the myosin head, causing it to detach from actin. Finally, ATP is hydrolyzed to ADP and inorganic phosphate. After that, the cycle may start again and another contraction may occur. The contraction and heart rate of the heart muscle is regulated by a process known as excitation-contraction coupling (ECC). During systole, depolarization of the plasma membrane opens the CTCL, resulting in an influx of a small amount of Ca2+ into the cell. This in turn induces the release of a large amount of Ca2+ from the SR via the ryanodine receptor in the Ca2+ induced ca2+ release. Soon after, intracellular Ca2+ levels increase 10-fold (from 100 nM to 1 μM) to reach the levels needed to bind toponin C and induce the conformational change needed to promote the actin-myosin-transverse bridge cycle (Frank et al., 2003; Maclennan and Kranias, 2003). At the onset of diastolic relaxation, Ca2+ dissociates troponin C, followed by readmission to SR by SR Ca2+ ATPase 2 (SERCA2) and distance from transsarcothema via the na2+/Ca2+ heat exchanger (NKX; Chakraborti et al., 2007). Heart rate is also regulated by the serca2 phospholamban (PLB) inhibitor, which is an important target for adrenergic signaling (Maclennan and Kranias, 2003). Thus, a strictly controlled cycle of Ca2+ input and release precisely regulates vibrations in the heart cells from beat to beat.
Viewed under a microscope, heart muscle cells are approximately rectangular and measure 100-150 μm by 30-40 μm. [8] Individual heart muscle cells are connected to each other at their extremities by intervertebral discs intercalated to form long fibers. Each cell contains myofibrils, specialized protein contraction fibers from actin and myosin that slide over each other. These are organized into sarcomeres, the basic contractile units of muscle cells. The regular organization of myofibrils into sarcomeres gives heart muscle cells a striped or scratched appearance when viewed under a microscope, similar to skeletal muscle. These streaks are caused by lighter I bands, which are mainly made up of actin, and darker A bands, mainly made up of myosin. [6] Myosin and Actin Animation: This animation shows myosin filaments (red) sliding along actin filaments (pink) to contract a muscle cell. Heart muscle cells form a highly branched cellular network in the heart.
They are connected from one end to the other by intervertebral discs intercalated and organized into layers of myocardial tissue wrapped around the chambers of the heart. The contraction of the individual cells of the heart muscle creates strength and shortening in these muscle ligaments, which leads to a decrease in the size of the ventricle and the resulting expulsion of blood into the lungs and vessels of the system. The important components of each heart muscle cell involved in the processes of excitation and metabolic recovery are the plasma membrane and transverse tubules in Z-line recording, the sarcoplasmic longitudinal reticulum and terminal cisterns, as well as mitochondria. Thick (myosin) and thin (actin, troponin and tropomyosin) protein filaments are arranged in contractile units, with the sarcomere extending from the Z line to the Z line, which have a characteristic striated pattern similar to that of skeletal muscles. Long QT type 1 syndrome (LQT1) is caused by mutations in the KCNQ1 gene, which codes for the formation of pores α subunit of the K+ channel of the slowly delayed rectifier. In phase 2 of the action potential, two different delayed rectifiers open K+ channels at different speeds, a fast delayed rectifier and a slow delayed rectifier. The slow, delayed rectifier channel consists of a α pore-forming subunit (KvLQT1) and a β subunit (MinK) encoded by the KCNE1 gene. LQT5 is caused by mutations in the KCNE1 gene. The K+ channel of the faster aperture delayed rectifier contains a α pore-forming subunit encoded by the HERG gene and a β subunit (MiRP1) encoded by the KCNE2 gene.
LQT2 is caused by mutations in the HERG gene and LQT6 is caused by mutations in the KCNE2 gene. Another type of K+ channel, an inward-facing rectifier K+ channel, plays little or no role in Phase 2 of the cardiac action potential, but is important during the Phase 3 repolarization phase. The current transmitted by these channels is called IK1 and is due to the inward-facing rectifier channel Kir2.1, which is encoded by the KCNJ2 gene. Reductions in IK1 prolong the repolarization phase of the action potential and mutations in KCNJ2 are based on LQT7. As discussed in the next section, Kir2.1 K+ channels are also expressed in skeletal muscle and mutations in KCNJ2 lead to a form of periodic skeletal muscle paralysis called Andersen syndrome (Andersen-Tawil syndrome). All forms of long QT syndrome caused by mutations in genes encoding K+ channel subunits are loss of function mutations that lead to a reduction in repolarization currents. This reduction in repolarization prolongs Phase 2 of the action potential, which is manifested by a longer QT interval on the ECG. Heart muscle contracts in the same way as skeletal muscle, although with some important differences.
Electrical stimulation in the form of a cardiac action potential triggers the release of calcium from the cell`s internal calcium reserve, the sarcoplasmic reticulum. The increase in calcium causes the cell`s myofilaments to slide on top of each other in a process called excitation-contraction coupling. Diseases of the heart muscle known as cardiomyopathies are of great importance. These include ischemic conditions caused by limited blood supply to the muscle, such as angina pectoris and myocardial infarction. It has been widely accepted that heart muscle cells cannot be regenerated. However, this was refuted by a report published in 2009. [24] Olaf Bergmann and colleagues at the Karolinska Institute in Stockholm tested heart muscle samples from people born before 1955 who had very little heart muscle around the heart, many presenting with disabilities due to this abnormality. Using DNA samples from many hearts, the researchers estimated that a 4-year-old child renews about 20 percent of heart muscle cells per year and about 69 percent of a 50-year-old man`s heart muscle cells were created after birth. [24] Calcium is no longer bound to troponin C and the actin binding site is hidden, stopping the contraction and relaxing the muscle.
To coordinate the contraction of cardiomyocytes in the heart, the action potentials between the cells must be distributed by lacunar junctions. .
