Calcium skeletal

The disorders of calcium homeostasis are related to the calcium content of the extracellular fluid, which contains less than 0.5% of the total body stores of calcium. Skeletal bone contains more than 99% of total body stores of calcium. ECF calcium is moderately bound to plasma proteins (46%), primarily albumin. Unbound or ionized calcium is the physiologically active form and is the fraction that is homeostatically regulated. Extracellular calcium, however, is most commonly measured as the total serum calcium level, which includes both bound and unbound calcium. The normal total calcium serum concentration range is 8.5 to 10.5 mg/dL. °... 

Adult osteomalacia often has an insidious presentation. " " The underlying disorder may be more apparent than skeletal defects (e.g., diarrhea in sprue). Diffuse skeletal pain, bony tenderness, and proximal muscle weakness may occur. Pain on movement and muscle weakness may result in a characteristic waddling gait. Hypophosphatemia and secondary hyperparathyroidism may contribute to these symptoms. Tetany can result from sufficiently depressed serum ionized calcium. Skeletal deformities (infrequent in adults) include leg bowing, pigeon chest, scoliosis, kyphosis, and shortening of the spine. 

Cohn SH, Gusmano EA. 1967. Kinetics of strontium and calcium skeletal metabolism in the rat. Proc Soc Exp Biol Med 126 79-83. 

Cohn SH, Bozzo SR, Jesseph JE, et al. 1966. Strontium and calcium skeletal discrimination determined by compartmental analysis. J Appl Physiol 21 67-72. 

Biogenic Ma.teria.ls, Deep ocean calcareous or siUceous oo2es are sediments containing >30% of biogenic material. Foraminifera, the skeletal remains of calcareous plankton, are found extensively in deep equatorial waters above the calcium carbonate compensation depth of 4000 to 5000 m. 

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. 

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. 

PTH is the most important regulator of bone remodelling and calcium homeostasis. PTH is an 84-amino acid polypeptide and is secreted by the parathyroid glands in response to reductions in blood levels of ionised calcium. The primary physiological effect of PTH is to increase serum calcium. To this aim, PTH acts on the kidney to decrease urine calcium, increase mine phosphate, and increase the conversion of 25-OH-vitamin D to l,25-(OH)2-vitamin D. PTH acts on bone acutely to increase bone resorption and thus release skeletal calcium into the circulation. However, due to the coupling of bone resorption and bone formation, the longer-term effect of increased PTH secretion is to increase both bone resorption and bone formation. 

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. 

Calsequestrin is the major calcium storage protein of the sarcoplasmic reticulum in skeletal and cardiac muscles. It is highly acidic and has a large capacity for Ca2+. Calsequestrin functions to localize calcium near the junctional face of the terminal cistemae from which calcium can be released into the cytosol via the ryanodine receptor. 

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. 

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