In muscle contraction

Calcium plays an important part in structure-building in living organisms, perhaps mainly because of its ability to link together phosphate-containing materials. Calcium ions in the cell play a vital part in muscle contraction. 

Soluble Compounds. The mechanism of barium toxicity is related to its ability to substitute for calcium in muscle contraction. Toxicity results from stimulation of smooth muscles of the gastrointestinal tract, the cardiac muscle, and the voluntary muscles, resulting in paralysis (47). Skeletal, arterial, intestinal, and bronchial muscle all seem to be affected by barium. 

Calcium is the trigger behind the muscle contraction process (24,25). Neural stimulation activates the release of stored Ca(Il) resulting in a dramatic increase in free calcium ion levels. The subsequent binding of Ca(Il) resulting in a dramatic increase in free calcium ion levels. The subsequent binding of Ca(Il) to the muscle protein troponin C provides the impetus for a conformational change in the troponin complex and sets off successive events resulting in muscle contraction. 

In the presence of calcium, the primary contractile protein, myosin, is phosphorylated by the myosin light-chain kinase initiating the subsequent actin-activation of the myosin adenosine triphosphate activity and resulting in muscle contraction. Removal of calcium inactivates the kinase and allows the myosin light chain to dephosphorylate myosin which results in muscle relaxation. Therefore the general biochemical mechanism for the muscle contractile process is dependent on the avaUabUity of a sufficient intraceUular calcium concentration. 

Huxley, A.F. Niedergerke, R. (1954). Structural changes in muscle contraction. Interference microscopy of living muscle fibres. Namre 173, 971-973. 

Ruegg, J.C. (1988). Calcium in Muscle Contraction. 2nd edn., Springer-Verlag, Heidelberg. 

The ability of S-2 to act as a flexible link also explained another problem in muscle contraction. When muscle contracts its volume remains constant. As a muscle shortens, and the filaments slide past each other, the spacing between the filaments increases as part of this constant volume behavior. Therefore, the crossbridges have to be able to interact with actin over a wide range of filament spacings. The presence of the flexible link in S-2 would allow this to occur. 

Kosower, E.M. (1970). A role for glutathione in muscle contraction. Experientia 26, 760-761. 

Slow-wave potentials also involve gradual depolarization of the cell membrane, but these depolarizations do not necessarily reach threshold. Therefore, the depolarization may simply be followed by repolarization back to the initial membrane potential. These slow "wave-like" potentials occur rhythmically and do not lead to smooth muscle contraction. The peak-to-peak amplitude of the slow-wave potential is in the range of 15 to 30 mV. Therefore, under the appropriate conditions, the depolarization phase of the slow-wave potential may, in fact, reach threshold. When this occurs, a burst of action potentials is generated, resulting in muscle contraction. 

Magnesium has its role intimately intertwined with phosphate in many phosphoryl transfer reactions, as Mg-ATP in muscle contraction, in the stabilization of nucleic acid structures as well as in the catalytic activity of ribozymes (catalytic RNA molecules). It also serves as a structural component of enzymes, and is found as the metal centre in chlorophylls, which absorbs light energy in photosynthesis. 

In 1931 Lundsgaard suggested that the energy used in muscle contraction was derived from phosphate bond energy supplied by glycolysis or respiratory oxidation. 

Like nitric oxide, the discovery of the eicosanoid signalling molecules was a significant event in twentieth century physiology, due largely to research led by Sir John Vane (Nobel Prize 1982). The diverse actions of the eicosanoids include roles in muscle contraction, blood coagulation, salt and fluid homeostasis, inflammatory responses and pain sensitivity. 

Some sarco(endo)plasmic reticulum (SR) Ca +-ATPases (SERCA) are P-type ATPases that play a major role in muscle contraction-relaxation cycles and are responsible for transporting calcium into the lumen of the sarcoplasmic reticulum. Some definitions are useful in the discussion of Ca +-ATPases ... 

The sliding filament model describes the mechanism involved in muscle contraction. In this model, sarcomeres become shorter when the thin and thick filaments slide alongside each other and telescope together, with ATP being consumed. During contraction, the following reaction cycle is repeated several times ... 

Amlodipine is a calcium channel blocker used to treat hypertension and angina pectoris. Calcium channel blockers block the passage of calcium, an essential factor in muscle contraction, into the heart and smooth muscles. Such blockage interferes with the contraction of these muscles, which in turn dilates the veins that supply blood to them. This reduces blood pressure. 

White, D. C. S., Wilson, M. G. A., Thorson, J. In Cross-bridge Mechanism in Muscle Contraction (eds. Sugi, H., Pollack, G. H.) University Park Press, Baltimore (1979)... 

Figure 16.4 Schematic representation of the stages in muscle contraction. The box on the right indicates the species bound to the myosin at each stage of the cycle. From Biochemistry, 4th Edition, by Stryer, p. 399. 1995, 1988, 1981, and 1975 by Lubert Stryer. Used with permission by W. H. Freeman and Company.

Weber, A., and Murray, J. M. (1973). Molecular control mechanisms in muscle contraction. Physiol. Rev. 53, 612-673. 

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