Hypo-osmotic shock of tobacco cells stimulates Ca2+ fluxes deriving first from external and then internal Ca2+ stores

Stephen G. Cessna, Sreeganga Chandra, Philip S. Low

Research output: Contribution to journalArticlepeer-review

63 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)27286-27291
Number of pages6
JournalJournal of Biological Chemistry
Issue number42
StatePublished - Oct 16 1998

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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