Calcium dependence of hypoosmotically induced potassium release in cultured astrocytes

Alex S. Bender, Michael D. Norenberg

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

A major mechanism in cell volume regulation after hypoosmotic stress is K+ release. Our studies show that in astrocytes, K+ release during hypoosmotic stress is a Ca2+-dependent process. Agents that increase intracellular Ca2+, such as ionomycin and ouabain, potentiated hypoosmotically stimulated K+ release, while compounds that block Ca2+ entry during hypoosmotic stress, such as nimodipine, bepridil, and MK-801, inhibited hypoosmotically stimulated K+ release. Similarly, chelation of intracellular Ca2+ blocked hypoosmotically induced K+ release. Caffeine and U-73122 also inhibited K+ efflux under hypoosmotic conditions, suggesting that intracellular Ca2+ release from Ca2+-induced Ca2+ release stores and inositol trisphosphate-sensitive intracellular Ca2+ stores play a role in the mechanism of K+ release. Blocking the activity of calmodulin, and of CaM kinase, attenuated hypoosmotically induced K+ release. Our findings indicate that entry of extracellular Ca2+ and Ca2+ release from intracellular stores play a key role in the activation of K+ release under hypoosmotic conditions and thus in cell volume regulation.

Original languageEnglish (US)
Pages (from-to)4237-4243
Number of pages7
JournalJournal of Neuroscience
Volume14
Issue number7
DOIs
StatePublished - Jul 1994

Keywords

  • astrocytes
  • calcium
  • hypoosmotic stress
  • potassium
  • volume regulation

ASJC Scopus subject areas

  • Neuroscience(all)

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