Calcium pools

J Llopis, GEN Kass, SK Duddy, GA Moore, S Orrenius. (1991). Mobilization of hormone sensitive calcium pool increases hepatocyte tight junctional permeability in the perfused rat liver. FEBS Lett 280 84-86. 

Long RM, Moore L. 1986b. Inhibition of liver endoplasmic reticulum calcium pump by CCH and release of a sequestered calcium pool. Biochem Pharmacol 35 4131-4137. 

Fig. 2. Effect of calcium antagonists (CA) on a cardiac cell. Top typical cardiac action potential. The calcium (slow) inward current flows during the characteristic plateau phase (phase 2) of the action potential. This calcium influx is selectively inhibited by CA. Activation of the sarcoplasmic reticulum (SR) and other cellular calcium pools occurs via Ca + and Na+ ions which flow into the cell. The SR and other pools donate activator Ca + ions which stimulate the contractile proteins. The presence of tubular systems (invaginations), which are characteristic of cardiac tissues, results in considerable enlargement of the cellular surface, thus enabling an effective influx of Na+ and Ca + ions. Inhibition of the calcium inward flux by a CA causes diminished activation of the contractile proteins.

Studies of the efflux of Ca by stimulated rabbit atria have characterized three calcium pools. Phase I may represent extracellular washout of the Ca that binds to the surface of muscle membrane and is characterized by a high rate constant. Phase II may represent loosely bound calcium present in cell membrane and calcium released at the sarcoplasmic reticulum. Calcium in this pool is directly related to contractility.65,84,93 phase III may represent the tightly bound calcium that exchanges very slotrly and does not play a role in maintaining calcium concentrations. Recent study has shown that the storage or release of calcium at the sarcoplasmic reticulum and other loosely bound calcium sites (cell membrane) that are involved in muscle contractility can be directly affected by 2-PAM.21 These results Indicate that 2-PAM increases the rate of release of Phase II calcium. 

Fitzgerald et al,54 studied the monitoring of calcium metabolism in patients in the final stages of renal disease using serum by AMS after isotopic labelling with a 41 Ca radiotracer. The authors hypothesized that bone resorption can be studied directly by serial measurements of the 41Ca/Ca,otal ratio in serum after in vivo labelling of the calcium pool with 41 Ca.54... 

The enzyme functions as a kind of chemical homeostaf by releasing calcium and carbonate to the extrapallial fluid from the reserves present in the mantle tissue. Because of the extreme sensitivity of the carbonate system to slight changes in pH (see p. 19, Fig. 14), carbonic anhydrase must operate in both directions in order to maintain a dynamic equilibrium between the bound and free calcium pools. 

Superimposed on these records are markings of environmental perturbations which sometimes inhibit, and sometimes accelerate carbonate deposition. In the final analysis, however, there has to be an answer, why organisms respond in such a systematic fashion. In all probability these phenomena are connected to the high demand for calcium at all levels of the cell regulatory system. Only at times of lower activities or when the calcium pool runs over will the excretory system package and export the surplus calcium to the periphery of the cell where it may be utilized in carbonate deposition. 

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-... 

The mitochondrial Ca2+ pool plays a second role in cellular Ca2+ homeostasis by serving as a sink for Ca2+ during times of excessive Ca2+ uptake by the cell. Under this circumstance, the non-ionic calcium pool in the matrix space can increase 10-fold or more, thereby protecting the cell from Ca2+ intoxication. This mechanism provides a temporary device by which the cell can protect itself, but in the long term only by regulating Ca2+ fluxes across the plasma membrane can the cell maintain Ca2+ homeostasis [14]. 

Fig. 3. The interrelated changes in the metabolism of phosphatidylinositol 4,5-bisphosphate (PIP2) and Ca2+ during activation of the cell by a typical Ca2+-dependent hormone. R, receptor G, guanine regulatory protein PLC, phospholipase C DG, diacylglycerol CK, protein kinase C [Ca2+]sm, the Ca2+ concentration in a cellular domain just beneath the plasma membrane (striped area) Insl,4,SP3, inositol 1,4,5-trisphosphate Insl,3,4,5P4, inositol 1,3,4,5-tetrakisphosphate [Ca2+]c, cytosolic Ca2+ concentration CaM, calmodulin arrows (=>), fluxes of Ca2+ across membranes s=>, energy-dependent fluxes CaY, a calcium pool in specialized compartment of the endoplasmic reticulum. See text for discussion.

Luo X, He Q, Huang Y, Sheikh MS (2005) Transcriptional upregulation of PUMA modulates endoplasmic reticulum calcium pool depletion-induced apoptosis via Bax activation. Cell Death Differ 12 1310-1318... 

Brune B, and Ullrich V. (1991). Differential calcium pools in human platelets and their role in thromboxane A formation. J. Biol. Chem 266,19232-19237. 

I, 4,5-trisphosphate-sensitive and insensitive calcium pools. Nature, 340, 236-239. 

C signal transduction pathway. Secretion of calcitonin is stimulated by hypercalcemia but the effect of the hormone on calcium transport appears to be secondary to increased phosphate uptake by target cells. The number and activity of osteoclasts are decreased, and urinary excretion of hy-droxyproline is decreased, Calcitonin may also inhibit release of calcium from the extracellular fluid calcium pool, but it increases calcium and phosphate excretion by renal tubules. Some tubular cells respond to calcitonin, PTH, and vasopressin, while others respond only to one or two of these hormones. In general, the actions of calcitonin in kidney and in bone are antagonistic to those of PTH. Calcitonin decreases secretion of gastrin and of gastric acid, and inhibits bile flow. 

Mi, S. et al., Study on calcium absorptivity in calcium supplements evaluated by 41Ca labeled calcium pool of osteoporotic rats, Acta Nutrim. Sin., 30( 1), 39, 2008. 

Studies on skeletal muscle also support an intracellular site of action of the MDIs. Thus, pr-MDI (10 4m) significantly blocked caffeine-induced contractures of the rat diaphragm both in presence and in absence of extracellular calcium (33). Such caffeine-induced contractures are believed to be mediated by intracellular calcium mobilized from the sarcoplasmic reticulum or other intracellular calcium pool (34). Furthermore, bu-MDI (10 M) depresses activation heat in the frog sartorius muscle upon stimulation (35), indicating a reduction in the quantity of calcium released from the sarcoplasmic reticulum, since activation heat represents the energy liberated in association with calcium mobilization and sequestration in contracting muscle (36,... 

Dolor, R., L. Hurwitz, Z. Mirza, H. Strauss R. Whorton. 1992. Regulation of extracellular Ca entry in endothelial cells role of intracellular calcium pool. J. Am. Physiol 262 C171-C181. 

It is well documented that N-formyl peptides induce a rapid, transient rise in intracellular calcium in neutrophils. It is also well established that inositol 1,4,5-trisphosphate released by the action of PLC triggers the release of Ca from intracellular stores. With the exception of the specific condition of neutrophils migrating on fibronectin and vitronectin [91], migration appears to occur in the absence of the intracellular calcium transient [196, 299, 456]. However, the studies that demonstrated this conclusion utilized indicators and buffers of cytosolic calcium that may not probe the entire calcium pool. Evidence suggests two additional mechanisms for regulating calcium that may have an impact on cell migration. 

Korchak, J.M., Vienne, K., Wilkenfeld, C., Roberts, C.S., Rutherford, L.E., Haines, K.A. and Weissmann, G. (1983). The role of calcium in neutrophil activation—mobilization of multiple calcium pools. J. Cell Biol. 97, 160a. 

The principal effect of calcitonin is to inhibit bone resorption by osteoclasts and this is reflected in a decreased excretion of hydroxyproline in the urine. Like PTH it acts on the stable calcium pool. Tissue culture preparations of bone, to which PTH has been added, show resorption but, if calcitonin is also added, resorption is inhibited. There is no evidence to support the idea that calcitonin promotes the deposition of bone. 

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