Ca2+ uptake in GH3 cells during hypotonic swelling: The sensory role of stretch-activated ion channels

Ye Chen-Izu, Steven M. Simasko, Jeffrey Niggel, Wade J. Sigurdson, Frederick Sachs

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

Hypotonic cell swelling triggers an increase in intracellular Ca2+ concentration that is deemed responsible for the subsequent regulated volume decrease in many cells. To understand the mechanisms underlying this increase, we have studied the Ca2+ sources that contribute to hypotonic cell swelling-induced Ca2+ increase (HICI) in GH3 cells. Fura 2 fluorescence of cell populations revealed that extracellular, but not intracellular, stores of Ca2+ were required. HICI was abolished by nifedipine, a blocker of L-type Ca2+ channels, and Gd3+, a nonspecific blocker of stretch-activated channels (SACs), suggesting two components for the Ca2+ membrane pathway: L-type Ca2+ channels and SACs. Using HICI as an assay, we found that venom from the spider Grammostola spatulata could block HICI without blocking L-type Ca2+ channels. The venom did, however, block SAC activity. This suggests that Ca2+-permeable SACs, rather than L- type Ca2+ channels, are the sensing elements for HICI. These results support the model for volume regulation in which SACs, activated by an increase of the membrane tension during hypotonic cell swelling, trigger HICI, leading to a volume decrease.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume270
Issue number6 39-6
StatePublished - Jun 1996
Externally publishedYes

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Keywords

  • blocker
  • gadolinium
  • Grammostola spatulata
  • inositol 1,4,5-trisphosphate-sensitive stores
  • L-type calcium channels
  • nifedipine
  • regulated volume decrease
  • spider venom
  • stretch-activated channels
  • thyrotropin-releasing hormone
  • volume regulation

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology
  • Physiology (medical)

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