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Sarcoplasmic reticulum, calcium

Source of calcium Sarcoplasmic reticulum Extracellular fluid (most) sarcoplasmic reticulum (some) Extracellular fluid (most) sarcoplasmic reticulum (some)... [Pg.156]

Keywords calcium, sarcoplasmic reticulum, cardiomyopathy, mutations... [Pg.523]

Contraction of muscle follows an increase of Ca " in the muscle cell as a result of nerve stimulation. This initiates processes which cause the proteins myosin and actin to be drawn together making the cell shorter and thicker. The return of the Ca " to its storage site, the sarcoplasmic reticulum, by an active pump mechanism allows the contracted muscle to relax (27). Calcium ion, also a factor in the release of acetylcholine on stimulation of nerve cells, influences the permeabiUty of cell membranes activates enzymes, such as adenosine triphosphatase (ATPase), Hpase, and some proteolytic enzymes and facihtates intestinal absorption of vitamin B 2 [68-19-9] (28). [Pg.376]

Another mechanism in initiating the contraction is agonist-induced contraction. It results from the hydrolysis of membrane phosphatidylinositol and the formation of inositol triphosphate (IP3)- IP3 in turn triggers the release of intracellular calcium from the sarcoplasmic reticulum and the influx of more extracellular calcium. The third mechanism in triggering the smooth muscle contraction is the increase of calcium influx through the receptor-operated channels. The increased cytosolic calcium enhances the binding to the protein, calmodulin [73298-54-1]. [Pg.141]

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. [Pg.555]

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. [Pg.397]

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. [Pg.314]

Sarcoplasmic calcium ATPase this enzyme utilizes the energy gained from hydrolysis of ATP to pump calcium from the cytosol into the stores of the sarcoplasmic reticulum. Its activity is negatively regulated by the closely associated protein phospholamban, and this inhibition is relieved upon phosphorylation of phospholamban by protein kinase A (PKA). [Pg.1119]

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... [Pg.219]

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... [Pg.224]

Sarcoplasmic reticulum Ca -channels. In many smooth muscle cells the rise of intracellular calcium which triggers contraction comes from the flow of calcium from the SR through Ca channels. In others, the SR contributes some unknown fraction of the triggering calcium relative to the amount which comes from the extracellular space through the plasma membrane Ca -channels. There are at least two kinds of Ca -channels in the SR. [Pg.189]

Figure 2. Muscle stimulation, a) a single nerve impulse (stimulus) causes a single contraction (a twitch). There is a small delay following the stimulus before force rises called the latent period, b) A train of stimuli at a low frequency causes an unfused tetanus. Force increases after each progressive stimulus towards a maximum, as calcium levels in the myofibrillar space increase. But there is enough time between each stimulus for calcium to be partially taken back up into the sarcoplasmic reticulum allowing partial relaxation before the next stimulus occurs, c) A train of stimuli at a higher frequency causes a fused tetanus, and force is maximum. There is not enough time for force to relax between stimuli. In the contractions shown here, the ends of the muscle are held fixed the contractions are isometric. Figure 2. Muscle stimulation, a) a single nerve impulse (stimulus) causes a single contraction (a twitch). There is a small delay following the stimulus before force rises called the latent period, b) A train of stimuli at a low frequency causes an unfused tetanus. Force increases after each progressive stimulus towards a maximum, as calcium levels in the myofibrillar space increase. But there is enough time between each stimulus for calcium to be partially taken back up into the sarcoplasmic reticulum allowing partial relaxation before the next stimulus occurs, c) A train of stimuli at a higher frequency causes a fused tetanus, and force is maximum. There is not enough time for force to relax between stimuli. In the contractions shown here, the ends of the muscle are held fixed the contractions are isometric.
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. [Pg.279]

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. [Pg.402]

Dantrolene is the mainstay of MH treatment. It has long been available for the treatment of muscle spasm in cerebral palsy and similar diseases. It is a hydantoin derivative that was first synthesized in 1967, and reported to be effective in the treatment of porcine MH in 1975. Also in 1975, dantrolene was shown to be more effective than procainamide in the treatment of human MH, which until that time was the drug of choice. However, the intravenous preparation was not made available until November 1979. It significantly lowered mortality. The half-life of dantrolene is estimated to be 6-8 hr. Dantrolene s primary mode of action is the reduction in calcium release by the sarcoplasmic reticulum. Dantrolene also exerts a primary antiarrhythmic effect by increasing atrial and ventricular refractory periods. Side effects of dentrolene include hepatotoxicity, muscle weakness, ataxia, blurred vision, slurred speech, nausea, and vomiting. Dantrolene is not contraindicated in pregnancy, but it does cross into breast milk and its effect on the neonate is unknown. [Pg.406]

Flubendiamide is an example of a new chemical class of insecticides that have been termed phthalic acid diamides (Nauen 2006, Copping and Duke 2007). They are related to the alkaloid ryanodine, which is extracted from Ryania species. Ryanodine affects muscles by binding to calcium channels of the sarcoplasmic reticulum. Ca + ions act as intracellular messengers, and their flux is modulated by calcium channels of this type. The toxic action of ryanodine and synthetic insecticides related to it is due to the disturbance of calcium flux. [Pg.7]

The T2 site also became protected from tryptic hydrolysis after phosphorylation of the native or solubilized sarcoplasmic reticulum vesicles with inorganic phosphate in a calcium free medium in the presence of dimethylsulfoxide or glycerol [121,252]. Under these conditions the Ca -ATPase is converted into a covalent E2-P intermediate, that is analogous in conformation to the E2V intermediate formed in the presence of vanadate. In contrast to this, the T2 site in the stable phosphorylated Ca2E P intermediate generated by the reaction of the Ca -ATPase with chro-mium-ATP in the presence of Ca [178,253] was fully exposed to trypsin, just as it was in the nonphosphorylated Ca2Ei form. Therefore the phosphorylated intermediates show the same sensitivity to trypsin at the T2 site as the corresponding nonphosphorylated enzyme forms. [Pg.86]

Reactive oxygen species modify the structure and function of the cardiac sarcoplasmic reticulum calcium release channel. Cardioscience 2, 19-25. [Pg.71]

Shattock, M.J., Matsuura, H. and Hearse, D.J. (1991). Functional and electrophysiolc cal effects of oxidant stress on isolated ventricular muscle role for oscillatory calcium release from sarcoplasmic reticulum in arrhythmogenesis. Cardiovasc. Res. 25, 645-651. [Pg.72]

Trimm, J.L., Salama, G. and Abramson, J.J. (1986). Sulphydryl oxidation induces rapid calcium release from sarcoplasmic reticulum vesicles. J. Biol. Chem. 261, 16092-16098. [Pg.72]

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... [Pg.440]

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... [Pg.240]

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... [Pg.240]

Endo, M., Calcium release from the sarcoplasmic reticulum, Physiology Review, 57, 71, 1977. [Pg.252]

Endo, M., Tanaka, M., and Ogawa, Y., Calcium induced release of calcium from sarcoplasmic reticulum of skinned skeletal muscle fibers, Nature, 228, 34, 1970. [Pg.252]

Fabiato, A. and Fabiato, F., Calcium release from sarcoplasmic reticulum, Circ Research, 40, 119, 1977. [Pg.252]

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. [Pg.143]

Fast-twitch muscle fibers develop tension two to three times faster than slow-twitch muscle fibers because of more rapid splitting of ATP by myosin ATPase. This enables the myosin crossbridges to cycle more rapidly Another factor influencing the speed of contraction involves the rate of removal of calcium from the cytoplasm. Muscle fibers remove Ca++ ions by pumping them back into the sarcoplasmic reticulum. Fast-twitch muscle fibers remove Ca++ ions more rapidly than slow-twitch muscle fibers, resulting in quicker twitches that are useful in fast precise movements. The contractions generated in slow-twitch muscle fibers may last up to 10 times longer than those of fast-twitch muscle fibers therefore, these twitches are useful in sustained, more powerful movements. [Pg.149]

The amount of tension developed by a muscle fiber during tetanic contraction can be as much as three to four times greater than that of a single muscle twitch. The mechanism involved with this increased strength of contraction involves the concentration of cytosolic calcium. Each time muscle fiber is stimulated by an action potential, Ca++ ions are released from the sarcoplasmic reticulum. However, as soon as the these ions are released, a... [Pg.151]

The action potential easily penetrates all regions of these small cells. Therefore, smooth muscle does not have transverse tubules. Furthermore, smooth muscle cells have very little sarcoplasmic reticulum, so intracellular storage of calcium is limited. Instead, the calcium needed for contraction is obtained primarily from the extracellular fluid. The influx of Ca++ ions through their channels in the cell membrane stimulates the release of a small amount of Ca++ ions from the sarcoplasmic reticulum. [Pg.157]

Calcium ions are actively pumped back into the extracellular fluid as well as the sarcoplasmic reticulum. When the concentration of calcium falls below... [Pg.157]

Inositol triphosphate (IP3)-gated channels are also associated with membrane-bound receptors for hormones and neurotransmitters. In this case, binding of a given substance to its receptor causes activation of another membrane-bound protein, phospholipase C. This enzyme promotes hydrolysis of phosphatidylinositol 4,5-diphosphate (PIP2) to IP3. The IP3 then diffuses to the sarcoplasmic reticulum and opens its calcium channels to release Ca++ ions from this intracellular storage site. [Pg.161]

Increases in the concentration of calcium in the cytosol provides a signal that can initiate muscle contraction, vision, and other signaling pathways. The response depends on the cell type. In muscle, a transient rise in the cytosolic calcium levels (from opening calcium channels in the sarcoplasmic reticulum) causes contraction. This signaling in contraction is a direct consequence of electrical activation of the voltage-gated channel. [Pg.147]

Calpactins calectrin Calpain Calsequestrin Membrane-binding proteins (365) Protease controlling cell adhesion (366) Sequesters calcium within the sarcoplasmic reticulum when muscles relax (80,367)... [Pg.290]


See other pages where Sarcoplasmic reticulum, calcium is mentioned: [Pg.304]    [Pg.47]    [Pg.97]    [Pg.185]    [Pg.206]    [Pg.401]    [Pg.406]    [Pg.139]    [Pg.6]    [Pg.59]    [Pg.180]    [Pg.57]    [Pg.152]    [Pg.168]    [Pg.410]    [Pg.299]   
See also in sourсe #XX -- [ Pg.567 ]

See also in sourсe #XX -- [ Pg.567 ]

See also in sourсe #XX -- [ Pg.6 , Pg.567 ]




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