Skeletal muscle calcium

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 ... 

The answer is b. (A furray, pp 48-73. Scriver, pp 4571-4636. Sack, pp 3—17. Wilson, pp 101-120.) Calcium ions are the regulators of contraction of skeletal muscle. Calcium is actively sequestered in sarcoplasmic... 

Functional expression of chimeras of the skeletal and cardiac muscle Uj subunit in skeletal muscle cells from mdg mice showed that the cytoplasmic loop between repeats II and III determines the type of excitation-contraction coupling (Fig. 2). The loop from the skeletal muscle calcium channel Ujs supports contraction in the absence of calcium influx, whereas the loop from the cardiac calcium channel Ujc subunit induces contraction only in the presence of calcium influx (Tanabe etal., 1990). These results suggest that the loop between repeats II and III interacts with the ryanodine receptor in a tissue-specific manner. 

Eu JP, Sun J, Xu L, Stamler JS, Meissner G. The skeletal muscle calcium release channel coupled O2 sensor and NO signaling functions. Cell 2000 102 499-509. 

Belcastro, A.N., Skeletal muscle calcium-activated neutral protease (calpain) with exercise, J Appl Physiol, 74, 1381, 1993. 

The trigger for all musele eontraetion is an increase in Ca eoneentration in the vicinity of the muscle fibers of skeletal muscle or the myocytes of cardiac and smooth muscle. In all these cases, this increase in Ca is due to the flow of Ca through calcium channels (Figure 17.24). A muscle contraction ends when the Ca concentration is reduced by specific calcium pumps (such as the SR Ca -ATPase, Chapter 10). The sarcoplasmic reticulum, t-tubule, and sarcolemmal membranes all contain Ca channels. As we shall see, the Ca channels of the SR function together with the t-tubules in a remarkable coupled process. 

Gitelzon, G. I., Tugai, V. A., and Zakharchenko, A. N. (1990). Production of obelin, a calcium-activated photoprotein, from Obelia longissima and its application for registration of the calcium efflux from the fragmented sarcoplasmic reticulum of skeletal muscles. Ukr. Biokhim. Zh. 62 69-76. 

Perreault, C. L., Gonzalez-Serratos, FI., Litwin, S. E., and Morgan, J. P. (1992). A chemical method for intracellular loading of the calcium indicator aequorin in mammalian skeletal muscle. Proc. Soc. Exp. Biol. Med. 199 178-182. 

Sorcin (soluble resistance-related calcium binding protein) was isolated from multidrug-resistant cells and is expressed in a few mammalian tissues such as skeletal muscle, heart, and brain. In the heart, sorcin interacts with the ryanodine receptor and L-type Ca2+-channels regulating excitation in contraction coupling. 

Sandwich complexes nickel. 5, 35 Sapphyrins, 2, 888 demetallation, 2, 891 metallation, 2, 891 reactions, 2, 891 synthesis, 2, 889 Sarcoplasmic reticulum calcium/magnesium ATPase, 6, 566 skeletal muscle... 

Site symmetry symbols, I, 128 Six-coordinate compounds stereochemistry, 1, 49-69 Six-membered rings metal complexes, 2, 79 Skeletal muscle sarcoplasmic reticulum calcium pump, 6, 565 Slags... 

The smooth muscle cell does not respond in an all-or-none manner, but instead its contractile state is a variable compromise between diverse regulatory influences. While a vertebrate skeletal muscle fiber is at complete rest unless activated by a motor nerve, regulation of the contractile activity of a smooth muscle cell is more complex. First, the smooth muscle cell typically receives input from many different kinds of nerve fibers. The various cell membrane receptors in turn activate different intracellular signal-transduction pathways which may affect (a) membrane channels, and hence, electrical activity (b) calcium storage or release or (c) the proteins of the contractile machinery. While each have their own biochemically specific ways, the actual mechanisms are for the most part known only in outline. 

In the sarcoplasm of smooth muscle cells there is a membrane bound compartment usually referred to as the SR by analogy with skeletal muscle. However, it is not at all clear that the interior of these membrane-bound regions are continuous as they are in skeletal muscle. The primary properties of this system seem to be quite similar to those of the endoplasmic reticulum of many other cell types. In general, calcium is concentrated into the membrane-bound reticulum and then released to initiate the characteristic action of the cell. 

Smith, J.S., Coronado, R., Meissner, G. (1986). Single channel measurements of the calcium release charmel from skeletal muscle sarcoplasmic reticulum. J. Gen. Physiol. 88, 573-588. 

Tanabe, T., Takeshima, H., Mikami, A., Flockerzi, V., Takahashi, H., Kangawa, K., Kojima, M., Matsuo, H., Hirose, T., Numa, S. (1987). Primary structure of the receptor for calcium channel blockers from skeletal muscle. Nature 328, 313-318. 

Westerblad, H., Lee, J.A., Lamb, A.G., Bolsover, S.R., Allen, D.G. (1990). Spatial gradients of intracellular calcium in skeletal muscle during fatigue. Pfluegers Arch. 415, 734-740. 

Pathogenesis of MH is not completely understood. Skeletal muscle, however, is the one tissue in MH with proven abnormalities, and it is further thought that the basic defect that causes the syndrome lies in the calcium regulation system found within the myoplasm. For example, calcium transport function appears to be decreased in the sarcoplasmic reticulum, mitochondria, and sarcolemma. Thus, the suggestion has been made that MH is characterized by a generalized membrane defeet. 

An area of substantial current interest is the relationship between free-radical-induced damage to muscle and the role of calcium in contraction-induced damage. We have undertaken studies of isolated skeletal muscles to specifically look at this area. 

Jackson, M.J., Jones, D.A. and Edwards, RH.T. (1984). Experimental skeletal muscle damage the nature of the calcium-activated degenerative processes. Eur. J. Clin. Invest. 14, 369-374. 

Johnson, K., Sutcliffe, L., Edwards, RH.T. and Jackson, M.J. (1988). Calcium ionophore enhances the electron spin resonance signal from isolated skeletal muscle. Bitxhim. Biophys. Acta 964, 285-288. 

McArdle, A., Edwards, R.H.T. and Jackson, M.J. (1993). Calcium homeostasis during contractile activity of vitamin E deficient skeletal muscle. Proc. Nutr. Soc. 52, 83A. 

More than 99% of total body calcium is found in bone the remaining less than 1% is in the ECF and ICE Calcium plays a critical role in the transmission of nerve impulses, skeletal muscle contraction, myocardial contractions, maintenance of normal cellular permeability, and the formation of bones and teeth. There is a reciprocal relationship between the serum calcium concentration (normally 8.6 to 10.2 mg/dL [2.15 to 2.55 mmol/L]) and the serum phosphate concentration that is regulated by a complex interaction between parathyroid hormone, vitamin D, and calcitonin. About one-half of the serum calcium is bound to plasma proteins the other half is free ionized calcium. Given that the serum calcium has significant protein binding, the serum calcium concentration must be corrected in patients who have low albumin concentrations (the major serum protein). The most commonly used formula adds 0.8 mg/dL (0.2 mmol/L) of calcium for each gram of albumin deficiency as follows ... 

Second-line Dantrolene Direct inhibitor of muscle contraction by decreasing the release of calcium from skeletal muscle sarcoplasmic reticulum 25 mg orally daily, increase to 25 mg 3-4 times daily, then increase by 25 mg every 4-7 days to a maximum of 400 mg/day... 

Three major mechanisms of action have dominated as possible explanations for the ergogenic potential of caffeine in the enhancement of exercise performance. These three mechanisms involve (1) the mobilization of intracellular calcium from the sarcoplasmic reticulum of skeletal muscle, (2) the increase of cyclic-3 ,5 -adenosine monophosphate (cAMP) by the inhibition of phosphodiesterases in muscles and adipocytes, and (3) the competitive antagonism of adenosine receptors, primarily in the central nervous system (CNS).8 9... 

For over three decades, laboratory research has shown caffeine to be effective at mobilizing calcium in skeletal muscle. In vitro experiments have amply demonstrated that caffeine lowers the excitability threshold and extends the length of muscular contractions via calcium release from the sarcoplasmic reticulum.1012 Caffeine also inhibits calcium reuptake by the sarcoplasmic reticulum, perpetuating calcium availability for muscle work.1318 Also, caffeine promotes increased twitch tension development in muscles.1718... 

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