Calcium uptake pathways

In the adrenal the All-regulated calcium uptake pathway has been extensively characterized. All-induced calcium influx into glomerulosa cells is dependent on the concentration of extracellular potassium within the range 2 to 8 mM and with a threshold value of 2 mM [47], Because glomerulosa cells are exquisitely sensitive... 

Soriano, M.E., Nicolosi, L., and Bernardi, P., 2004, Desensitization of the permeability transition pore by cyclosporin A prevents activation of the mitochondrial apoptotic pathway and liver damage by tumor necrosis factor-alpha, J. Biol. Chem. 279, pp. 36803-36808 Sparagna, G.C., Gunter, K. K., Sheu, S. S., and Gunter, T. E., 1995, Mitochondrial calcium uptake from physiological-type pulses of calcium. A description of the rapid uptake mode, J. Biol. Chem. 270, pp. 27510-27515... 

Cannabinoids may also cause effects via mechanisms distinct from the cannabinoid receptor pathways. The most extensively investigated compound is (+)-HU 211, a synthetic cannabinoid with a stereochemistry opposite to that present in the naturally occurring compounds. It does not produce THC-type effects in animals and shows insignificant binding to the CB, receptor. However, HU 211 blocks A-methyl-n-aspartate (NMDA) receptors and calcium uptake through the NMDA-receptor-ion channel in primary cell cultures. HU 211 is a potent blocker of NMDA-induced tremor, seizures, and lethality in mice. It may therefore prove useful as a nonpsychoactive drug that protects against NMDA-receptor-mediated neurotoxicity. This is supported by the potent attenuation of NMDA-receptor-mediator neurotoxicity in cell cultures by HU 211. 

H)2D increases reabsorption of phosphate in the kidney and intestinal absorption of phosphate. In the intestine, phosphate is absorbed as a counterion with Ca + and also by a calcium-independent route. Phosphate flux through both pathways is increased by l,25-(OH)2D but more slowly than calcium transport. The calcium-independent pathway may involve alkaline phosphatase, the activity of which is increased by l,25-(OH)2D. In rat intestine in vitro, phosphate transport is greatest in the jejunum and least in the ileum, whereas calcium uptake is highest in the duodenum. 

The injection of human NGF caused mechanical sensitization that lasted for at least 3 hours however, there was no indication that human NGF produced these effects indirectly through local muscle inflammation. The peripheral effects of NGF are likely mediated through a receptor mechanism, for example, TrkA receptor mediated pathways [136]. It is possible that nonspecific mechanisms, such as foreign protein reactions, decreased degradation of human NGF by rat proteases, slowed clearance from the muscle, modulation of intracellular calcium concentration (calcium uptake) [137,138], actions on bradykinin receptors [139], capsaicin receptors [37,140], or sodium channels [141,142] might contribute to the effect of human NGF in rats. 

In that paper, we suggested for the first time that GA effects were related to inhibition of calcium uptake by smooth muscle and that indeed GA could be seen as a calcium channel blocker. This compoimd affected the contractile uterine responses in several species including human uterine smooth muscle [34]. GA also caused inhibition in the responses elicited by a number of spasmogenic compounds including acetylcholine, prostaglandins and even oxytocin "Fig. (5)." These drugs are known to enhance calcium influx by different but linked signal transduction pathways. 

The most common uptake pathway into the cell for nontargeted polymers occurs via passive endocytosis, and indeed has been shown to be the pathway for both PEI and PEL [59, 60]. It is also likely that transfection occurring via endocytosis takes place for many polymers through calcium mediated cell anchorage to the extracellular matrix. The normal... 

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. - ... 

The functions of the calcium-storage capacity of the ER are at least threefold the association of Ca2+ with Ca2+-binding proteins in the ER is part of a chaperone function that is essential for normal protein synthesis the rapid rate of Ca2+ uptake by endoplasmic pumps provides shortterm cytoplasmic Ca2+ buffering that resists untoward and transient changes in [Ca2+] and, finally, many signaling pathways employ elevated [Ca2+] to activate physiological processes. Extensive Ca2+ release from ER is coupled to activation of Ca2+ entry across the plasma membrane, a process known as capacitative calcium entry, which is discussed below. 

What has happened to the bicarbonate and calcium delivered to the ocean by river runoff As described later, these two ions are removed from seawater by calcareous plankton because a significant fraction of their hard parts are buried in the sediment. In contrast, the only sedimentary way out of the ocean for chloride is as burial in pore waters or precipitation of evaporites. The story with sodium is more complicated— removal also occurs via hydrothermal uptake and cation exchange. Because the major ions are removed from seawater by different pathways, they experience different degrees of retention in seawater and uptake into the sediments. Another level of fractionation occurs when the oceanic crust and its overlying sediments move through the rock cycle as some of the subducted material is remelted in the mantle and some is uplifted onto the continents. 

The catecholamines and serotonin share similar pathways of biosynthesis and metabolism, including in some steps, the same enzymes. Catecholamines and serotonin are sequestered and stored in vesicular granules from where they are released mto the extracellular environment by calcium-dependent exocytosis. Termination of the physiological effects of both the catecholamines and serotonin is dependent on active uptake processes, facilitated by specific... 

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. 

Lagged E, Akron K, Fonyo A. 1979. The inhibitor-sensitivity and pathways of uptake during calcium and strontium accumulation in liver mitochondria. FEBS Lett 107(l) 205-208. 

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