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Cytosolic calcium mobilization

Regarding human tissues, the few data available are contradictory, since according to some authors (Tedeschi et al., 1991) histamine release from basophils is not modified by H3 receptor ligands. In other studies (Bent et al., 1991), it was found that thioperamide could increase histamine release from adenoidal mast cells, but apparently (R)a-methylhistamine was totally inactive. In any case the concentrations of thioperamide are much higher than those necessary to block H3 receptors, thus suggesting that other mechanisms might be involved. Raible et al., (1994) hypothesized by the use of thioperamide, the presence of H3 receptors on human eosinophils which mediate histamine-induced increase in cytosolic calcium mobilization. However, the low efficacy of the known H3 receptor agonists, -as stimuli for eosinophils... [Pg.95]

Gelperin, D., Mann, D., Del Valle, J. and Wiley, J. Bradykinin (BK) increases cytosolic calcium in cultured rat myenteric neurons via BK-2 type receptors coupled to mobilization of extracellular and intracellular sources of calcium Evidence that calcium influx is prostaglandin dependent. /. Pharmacol. Exp. Ther. 271 507-514,1994. [Pg.183]

Although slightly attenuated, the rise in cytosolic calcium proceeds in the absence of extracellular calcium (as mentioned above), indicating that upon All stimulation calcium is released into the cytosol from an internal pool. The identity of this mobilized internal pool was initially inferred from cellular studies in which treatment with dantrolene inhibited the redistribution of intracellular calcium [39,40], Be-... [Pg.219]

Once mobilized, a large proportion of the cytosolic calcium load is extruded from the cell across the plasma membrane. This extrusion can be demonstrated by measuring the efflux of radiocalcium from previously labeled cells. All stimulation of adrenal, hepatic and vascular smooth muscle cells preloaded with radioactive calcium induces a marked increase in efflux of the radiolabel. This increased efflux is transient, peaking between 4 and 5 minutes after All addition and is observed in the absence of extracellular calcium [39]. Furthermore, under conditions of zero calcium, treatment of cells with dantrolene prior to hormonal stimulation abolishes the All-induced calcium efflux [40], confirming that the radiocalcium lost from the cell is mobilized from a component of the ER. [Pg.220]

Smith JB, Dwyer SD, Smith L (1989) Cadmium evokes inositol polyphosphate formation and calcium mobilization. J Biol Chem 264 7115-7118 Smith MW, Phelps PC, Trump BF (1991) Cytosolic Ca " deregulation and blebbing after HgCl2 injury to cultured rabbit proximal tubule cells as determined by digital imaging microscopy. Proc Natl Acad Sci USA 88 4926-4930 Smith RM, Martell AE (1976) Critical stability constants. Plenum, New York Stirling CE (1975) Mercurial perturbation of brush border membrane permeability in rabbit ileum. J Membr Biol 23 33-56... [Pg.75]

Kiang JG, Smallridge RC. 1994. Sodium cyanide increases cytosolic free calcium evidence for activation of the reversed mode of the Na+/Ca2+ exchanger and Ca2+ mobilization from inositol trisphosphate-insensitive pools. Toxicol Appl Pharmacol 127(2) 173-181. [Pg.256]

There are three important ADP receptors on the platelet surface (16). The P2X, inotrophic receptor is responsible for rapid influx of calcium into the cytosol. The P2Y, receptor mediates mobilization of calcium through activation of PLC and shape change. The P2Y,2 receptor is coupled to adenyl cyclase inhibition mediated by a G-protein with subsequent decrease in the cAMP The decrease in cAMP stimulates dephosphorylation of VASP that is closely correlated with the GPIIb/llla activation. [Pg.35]


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See also in sourсe #XX -- [ Pg.30 , Pg.339 ]

See also in sourсe #XX -- [ Pg.339 ]




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