Hypo-osmotic Shock of Tobacco Cells Stimulates Ca2+Fluxes Deriving First from External and then Internal Ca2+Stores

• Published in: The Journal of biological chemistry 1998-10, Vol.273 (42), p.27286-27291
• Main Authors: Cessna, Stephen G., Chandra, Sreeganga, Low, Philip S.
• Format: Article
• Language: English
• Subjects: Aequorin; ANTIMETABOLITE; ANTIMETABOLITES; ANTIMETABOLITOS; Biological Transport; Caffeine - pharmacology; CALCIO; CALCIUM; Calcium - metabolism; Calcium Channels - metabolism; Calcium Signaling; CATION; CATIONES; CATIONS; Cell Compartmentation; CELL CULTURE; CELL SUSPENSIONS; CITOPLASMA; COLORANT; COLORANTES; CULTIVO DE CELULAS; CULTURE DE CELLULE; CYTOPLASM; CYTOPLASME; CYTOSOL; Cytosol - metabolism; DYES; Egtazic Acid - pharmacology; ELEMENT CHIMIQUE; ELEMENTOS DE TIERRAS RARAS; ELEMENTOS QUIMICOS; ELEMENTS; ESTRES; GADOLINIUM RUTHENIUM RED; ION; Ion Channels - metabolism; ION TRANSPORT; ION UPTAKE; IONES; IONS; Kinetics; LANTHANUM; Lanthanum - pharmacology; MAGNESIO; MAGNESIUM; Magnesium - pharmacology; MANGANESE; MANGANESO; METAL DES TERRES RARES; Nicotiana - cytology; Nicotiana - metabolism; NICOTIANA PLUMBAGINIFOLIA; NIFLUMATE; Niflumic Acid - pharmacology; OSMOTIC PRESSURE; Plants, Toxic; PRESION OSMOTICA; PRESSION OSMOTIQUE; RARE EARTH ELEMENTS; REGULATION; RELEASE; Respiratory Burst; STRESS
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.273.42.27286

Hypo-osmotic shock of aequorin-transformed tobacco cells induces a biphasic cytosolic Ca2+influx. Because both phases of Ca2+ entry are readily blocked by Ca2+ channel inhibitors, we conclude that the Ca2+ transients are mediated by Ca2+ channels. Evidence that the first but not second Ca2+ transient derives from external Ca2+ stores is that the first but not second influx is (i) eliminated by membrane-impermeable Ca2+ chelators, (ii) enlarged by supplementation of the medium with excess Ca2+, and (iii) reduced by the addition of competitive cations such as Mg2+ and Mn2+. Furthermore, entry of 45Ca during osmotic shock is prevented by inhibitors of the first but not second phase of Ca2+ entry. Evidence that the second wave of Ca2+ influx stems from release of intracellular Ca2+ is based on the above data plus observations that probable modulators of intracellular Ca2+ channels selectively block this phase of Ca2+ influx. Finally, a mechanism of communication between the two Ca2+ release pathways has become apparent, since perturbations that elevate or reduce the first Ca2+ transient lead to a compensating diminution/elevation of the second and vice versa. These data thus suggest that osmotic shock leads to the sequential opening of extracellular followed by intracellular Ca2+ stores and that these Ca2+ release pathways are internally compensated.