Mechanism of contraction

All types of muscle require calcium for contraction. In skeletal muscle, Ca++ ions are stored within an extensive membranous network referred to as the sarcoplasmic reticulum. This network is found throughout the muscle fiber and surrounds each myofibril. Furthermore, segments of the sarcoplasmic reticulum lie adjacent to each T tubule that, with a segment of sarcoplasmic reticulum on either side of it, is referred to as a triad. As the action potential is transmitted along the T tubule, it stimulates the release of Ca++ ions from the sarcoplasmic reticulum. The only source of calcium for skeletal muscle contraction is the sarcoplasmic reticulum. 

In the absence of ATP, myosin crossbridges are unable to release the actin. As a result, the sarcomeres, and therefore the muscle, remain contracted. This phenomenon is referred to as rigor mortis. Following death, the concentration of intracellular calcium increases. This calcium allows the 

When the action potentials in the alpha motor neuron cease, stimulation of muscle fiber is ended. Ca++ ions are pumped back into the sarcoplasmic reticulum and troponin and tropomyosin return to their original positions. As a result, the myosin-binding sites on the actin are covered once again. The thin filaments return passively to their original positions, resulting in muscle relaxation. 

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In skeletal muscle, calcium binds to troponin and causes the repositioning of tropomyosin. As a result, the myosin-binding sites on the actin become uncovered and crossbridge cycling takes place. Although an increase in cytosolic calcium is also needed in smooth muscle, its role in the mechanism of contraction is very different. Three major steps are involved in smooth muscle contraction ... 

Organized into sarcomeres Sliding-filament mechanism of contraction Source of calcium ... 

Figure 13.5 Electron micrograph of part of a longitudinal section of a myofibril. Identification of components and the mechanism of contraction. When a muscle fibre is stimulated to contract, the actin and myosin filaments react by sliding past each other but with no change in length of either myofilament. The thick myosin strands in the A band are relatively stationary, whereas the thin actin filaments, which are attached to the Z discs, extend further into the A band and may eventually obliterate the H band. Because the thin filaments are attached to Z discs, the discs are drawn toward each other, so that the sarcomeres, the distance between the adjacent Z-discs, are compressed, the myofibril is shortened, and contraction of the muscle occurs. Contraction, therefore, is not due to a shortening of either the actin or the myosin filaments but is due to an increase in the overlap between the filaments. The force is generated by millions of cross-bridges interacting with actin filaments (Fig. 13.6). The electron micrograph was kindly provided by Professor D.S. Smith.

GAS eliminates the binding material (carbon) resulting in complete pellet destruction. The mechanism of contraction produced by GAS is not the reverse of elongation it is an extension of pellet destmction by another mechanism. Also, its dynamics are not zero in carbon content It is hypothesized that pellet contraction or failure produced by elimination of carbon may be described on the basis of a percolation model by numerical simulation method. 

A basic knowledge of the physiology of the heart, the mechanism of contraction, electrical activity and control of rate and rhythm, maintenance of blood pressure and what can go wrong is needed in order to understand how the drugs work. 

Mechanisms of contraction for mesenchymal cells may be more dependent on formation of stress fibers and focal contacts than on the cortical contraction mechanisms seen in Dictyostelium [195]. Receptor tyrosine kinases can stimulate increased myosin light chain phosphorylation via rho activation as a mechanism for contraction. Alternatively, increased contraction may follow formation of new focal contacts, possibly via focal adhesion kinase and src-based mechanisms [212]. This would be consistent with the temporal sequence of events that are observed, with contraction being a late step that should follow formation of new focal contacts. 

If one looks more closely at the situation, however, one cannot escape the feeling that the cross-bridge model has shifted the problem of finding the mechanism of contraction from the level of the myofilaments to the properties of the cross-bridges. These have to perform the (Maxwellian)... 

The Mechanism of Contraction of Muscle.—The assignment of the pleated-sheet configuration to extended muscle and of the a-helical configuration to contracted muscle suggests that a discussion be made of the mechanism of contraction of muscle. 

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