Calcium uptake by sarcoplasmic reticulum

Fig. 5. Calcium uptake of sarcoplasmic reticulum vesicles supported by different substrates followed by calcium release after substrate depletion113. The time courses of calcium uptake and calcium release were measured by flow dialysis. The reaction chamber contained 0.4 mg protcin/ml, 5 mM MgCl2,...

Fig. 10. The effect of different concentrations of the ionophore X 537 A on calcium release, by sarcoplasmic reticulum vesicles11S. The reaction mixture contained 20 mM Tris-maleate pH 6-8, 50 mM KC1, 10 mM MgClj, 0.1 mM CaCl2, 0.1 mM murexide and 0.27 mg protein/ml. Calcium uptake and release were followed by monitoring the changes in the absorbance undergone by murexide. The measurements were performed with a filter dual wave length (540—507 nm) double beam spectrophotometer...

It has been postulated that 2-PAM exerts its cardiac action in rabbit atria through its alteration of calcium metabolism. The relaxation phase of skeletal muscle contraction seems to be directly affected by the sarcoplasmic reticulum because of its ability to sequester calcium actively.29,46 a similar role has been suggested for the sarcoplasmic reticulum in cardiac muscle. 6,83 The onset of muscle contraction takes place when calcium reaches a crit-cal concentration. This contraction is later reduced by the increased calcium-sequestering activity of the sarcoplasmic reticulum. Thus, 2-PAM can affect this process by decreasing the rate of calcium uptake by the sarcoplasmic reticulum, which results in increasing the time required to reduce the calcium concentration enough to allow relaxation to take place. This was demonstrated by the Increase in the relaxation phase. It was suggested that this... 

Mermier P, Hasselbach W. 1976. Comparison between strontium and calcium uptake by the fragmented sarcoplasmic reticulum. Eur J Biochem 69 79-86. 

Figure 7.2. Some intracellular processes that may be affected by calcium channel blocking drugs. Calcium channel blocking drugs inhibit calmodulin-dependent sarcolemmal Ca2 -A TPase (7), myosin light-chain kinase (MLCK) (2) and phosphodiesterase (PDE) (7). Passive Na -Ca2 exchange (4) may also be inhibited, whilst (Na +K )-ATPase (J) is stimulated. Ca2 release from mitochondria (MIT) in exchange for Na ( ) may be inhibited, but the effect of calcium channel blocking drugs on Ca2 uptake into sarcoplasmic reticulum (SR) via Ca2 -ATPase (7) is variable.

The biochemical mechanism of action of digitalis is associated with (A) A decrease in calcium uptake by the sarcoplasmic reticulum... 

Incubation of rat aortic rings with palytoxin led to microvesiculation of the endothelial cell cytoplasm [87], Dilatation of the sarcoplasmic reticulum, densification of mitochondrial cristae (possibly reflecting calcium uptake by the tissue), and disruption of myofibrils were observed in isolated rat muscle [88], Addition of palytoxin to the perfusion medium of the perfused heart caused cardiac arrest within minutes [13], and the spontaneous beating of isolated rat auricles was rapidly inhibited [9],... 

Calcium overload is a ubiquitous phenomena associated with cellular oxidant stress, including photosensitization-induced stress. Ver Donck et al. were the first to demonstrate that photosensitization causes calcium overload-induced hypercontracture of the isolated cardiac ceU. Subsequent studies provided evidence that a variety of mechanisms play a role in photosensitization-induced calcium overload. These include inhibition of the sodium-potassium pump, the sodium—calcium exchanger, and calcium uptake by the sarcoplasmic reticulum. Inhibition of the sodium—potassium pump leads to increased intracellular sodium and subsequent reduction of calcium efflux via the sodium-calcium exchanger. Suppression of sodium-calcium exchange also reduces calcium efflux. Inhibition of calcium uptake by the sarcoplasmic reticulum increases free-ionized intracellular calcium concentration. Calcium influx also plays an important role in photosensitization-induced calcium overload. Photosensitization increases membrane permeability and produces an associated leak current. - The membrane conductance related to this leak current increases with time during photosensitization, does not require a rise in intracellular calcium for its activation, and provides a path for sodium and calcium influx and potassium efflux. Calcium influx via the membrane permeability pathway created by photosensitization produces a calcium-dependent hypercontracture of the isolated cardiac ceU at membrane conductances indicative of an intact membrane. It also plays a role in cell killing. - ... 

Batrachotoxin is extremely potent in antagonizing axonal transport 198). It would appear that the basis of the effect of batrachotoxin on axonal transport is dependent on interactions with sodium channels and the resultant influx of sodium ions. The effect is blocked by tetrodotoxin. In the mollusc, Aplysia californica, it has been proposed that the inhibition of axonal transport by batrachotoxin is not due to interactions with sodium channels 169), but this interpretation has been questioned 105). Blockade of axonal transport by batrachotoxin reduced uptake and transport of nerve growth factor at distal terminals 41), increased activity of certain muscle lysosomal enzymes 40), and altered uptake of calcium in muscle sarcoplasmic reticulum 264, 265). Batrachotoxin inhibits saltatory movements in neuroblastoma cells 105). This inhibitory effect is blocked by tetrodotoxin. 

Calcium uptake by muscle sarcoplasmic reticulum following neural application of... 

The sER also functions as an intracellular calcium store, which normally keeps the Ca level in the cytoplasm low. This function is particularly marked in the sarcoplasmic reticulum, a specialized form of the sER in muscle cells (see p. 334). For release and uptake of Ca " ", the membranes of the sER contain signal-controlled Ca channels and energy-dependent Ca ATPases (see p. 220). In the lumen of the sER, the high Ca " " concentration is buffered by Ca -binding proteins. 

The uptake of calcium is usually initiated by the addition of calcium ions to the otherwise complete assay medium. Before calcium is added, ATP is split with a low rate by most sarcoplasmic reticulum preparations. This ATPase which is active in the absence of calcium ions has been named basic ATPase . 

In muscle cells, the contraction is induced by Ca2+ release from the sarcoplasmic reticulum, as a result of membrane depolarization and activation of RyRl receptors located at the surface of the SR. The subsequent transport of cytoplasmic Ca2+ back into the lumen of the sarcoplasmic reticulum restores low resting calcium levels and allows muscle relaxation. In fast-twitch skeletal muscle fibers, Ca2+ uptake is mediated by the sarco(endo)plasmic reticulum Ca2+ ATPase SERCA1 which represents more than 99% of SERCA isoforms in these muscle fibers. 

It has become increasingly clear that there is a non-mitochondrial, intracellular calcium pool which plays an important role in cell activation in a large number of nonmuscle cells as well as in smooth and skeletal muscle. This pool is relatively enormous in skeletal muscle, provides the bulk of the Ca2+ needed to regulate skeletal muscle contraction, and is located in a distinct organelle, the sarcoplasmic reticulum. The pool is smaller in non-muscle and in smooth muscle cells, and its location less obvious [10,11]. To fill the pool requires ATP, i.e., uptake of Ca2+ into the pool is driven by a distinct Ca2+-ATPase, an enzyme which purifies with the mi-... 

An early report suggested that suramin can block the nucleotide-dependent calcium pump of rabbit skeletal sarcoplasmic reticulum by inhibition of the calcium uptake and the ATTase activity [51]. These results have been confirmed by Emmik et al. [52]. Baumert and Heider [53] found that pyridoxal-5-phosphate and a series of its analogues (for chemical structure. 

Larger coupling ratios can also erroneously be obtained when calcium uptake ceases before the splitting of ATP is interrupted. In this case, the calcium-dependent ATPase activity is underestimated. Similar deviations can be expected if the preparation contains an enzyme which transports calcium without being activated by calcium ions, as it is the case for sarcoplasmic reticulum preparations isolated from red skeletal muscles [34]. On the other hand, smaller ratios were found when the preparation contained a sizeable fraction of open vesicles this fraction only contributes to the calcium-dependent ATPase activity and not to calcium transport. A reduced coupling ratio can also result from an increase in calcium permeability occurring for instance, at elevated temperatures or at alkaline pH [72]. 

The techniques employed to measure the ATP dependent, azide insensitive calcium uptake at 25 by whole cell muscle homogenates and isolated SR are described elsewhere (Boland et al., 1974 Martonosi et al., 1976). The concentration of Ca-ATPase in homogenates and sarcoplasmic reticulum membranes was determined by specific labeling of the enz)mie with 32p-ATP (Martonosi et al., 1976). 

Ballatori N, Shi C, Boyer JL (1988) Altered plasma membrane ion permeability in mercury-induced cell injury studies in hepatocytes of elasmobranch Raja erinacea. Toxicol Appl Pharmacol 95 279-291 Benndorf K, Nilius B (1988) Different blocking effects of Cd and Hg on the early outward current in myocardial mouse cells. Gen Physiol Biophys 7 345-352 Blazka ME, Shaikh ZA (1991) Differences in cadmium and mercury uptakes by hepatocytes role of calcium channels. Toxicol Appl Pharmacol 110 355-363 Brunder DG, Dettbarn C, Palade P (1988) heavy metal-induced Ca " release from sarcoplasmic reticulum. J Biol Chem 263 18785-18792 Butler JN (1964) Introduction to complex formation equilibria. Ionic equilibrium, a mathematical approach. Addison-Wesley, Reading, Massachusetts Palo Alto London, p 261... 

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