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J. Biol. Chem., Vol. 269, Issue 38, 23597-23602, 09, 1994
A Gamberucci, B Innocenti, R Fulceri, G Banhegyi, R Giunti, T Pozzan and A Benedetti
The effects of a number of metabolic inhibitors on the influx of Ca2+
activated by stimulation of receptors coupled to inositol 1,4,5-
trisphosphate generation or by depletion of intracellular Ca2+ stores with
thapsigargin were investigated in four different cell types: Ehrlich
ascites tumor cells, Jurkat and HeLa cell lines, and rat hepatocytes.
Independently of their chemical structure and site of inhibition, all of
these metabolic poisons markedly inhibited Ca2+ influx without
significantly affecting Ca2+ release. This inhibition was not due to
membrane potential depolarization or to alteration in cytosolic pH but
appeared correlated to a drop in the cellular concentration of ATP. The
decreases in cellular [ATP] were paralleled by decreases in [GTP] and by
increases in [ADP] and [GDP]. The reduction in ATP level necessary to
drastically reduce Ca2+ influx was quite small, e.g. a 50% inhibition for a
5% reduction in [ATP], thus within the range of fluctuation presumably
occurring under physiological conditions. We suggest that changes in the
adenine or guanine nucleotide concentrations may represent an important
modulatory mechanism of Ca2+ influx activated by store depletion.
Modulation of Ca2+ influx dependent on store depletion by intracellular adenine-guanine nucleotide levels
Institute of General Pathology, University of Siena, Italy.
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