Calcium dependence of hypoosmotically induced potassium release in cultured astrocytes.
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 Ca(2+)-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 Ca(2+)-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.
Department of Pathology, University of Miami School of Medicine, Florida 33101.
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Bender
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Norenberg
D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002478:Cells, Cultured; D005110:Extracellular Space / Q000378:metabolism; D006706:Homeostasis; D007425:Intracellular Membranes / Q000378:metabolism; D009994:Osmolar Concentration; D009995:Osmosis; D011188:Potassium / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D012413:Rubidium / Q000378:metabolism; D012414:Rubidium Radioisotopes; D013268:Stimulation, Chemical
D012414:Rubidium Radioisotopes; D011494:Protein Kinases; D012413:Rubidium; D011188:Potassium; D002118:Calcium