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Related Experiment Videos

Regulatory volume decrease in Ehrlich ascites tumor cells is not mediated by a rise in intracellular calcium

R J Young1, T C Smith, C Levinson

  • 1Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.

Biochimica Et Biophysica Acta
|February 23, 1993
PubMed
Summary
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Calcium ions do not trigger regulatory volume decrease (RVD) in Ehrlich ascites tumor cells during hyposmotic stress. This study found no increase in intracellular calcium, and RVD was unaffected by calcium channel blockers.

Area of Science:

  • Cell biology
  • Physiology
  • Biochemistry

Background:

  • Ehrlich ascites tumor cells exhibit regulatory volume decrease (RVD) when exposed to hyposmotic conditions.
  • RVD involves the loss of KCl, but the underlying mechanism remains unclear.
  • A hypothesis suggested that increased intracellular calcium ([Ca2+]i) activates calcium-sensitive conductances to initiate RVD.

Purpose of the Study:

  • To investigate the role of intracellular calcium ([Ca2+]i) in initiating regulatory volume decrease (RVD) in Ehrlich ascites tumor cells.
  • To determine if calcium acts as a second messenger in the RVD process.

Main Methods:

  • Exposure of Ehrlich ascites tumor cells to hyposmotic solutions (180 mosM from 300 mosM).
  • Measurement of intracellular calcium ([Ca2+]i) levels.

Related Experiment Videos

  • Assessment of RVD in the presence of calcium-sensitive K+ channel blockers (charybdotoxin and nifedipine).
  • Induction of cell shrinkage using the ionophore ionomycin.

    • Main Results:

    • No significant rise in intracellular calcium ([Ca2+]i) was observed in Ehrlich cells during hyposmotic stress.
    • Regulatory volume decrease (RVD) was not inhibited by charybdotoxin or nifedipine.
    • Ionomycin induced cell shrinkage sensitive to charybdotoxin and nifedipine, suggesting a different calcium-mediated mechanism.

    Conclusions:

    • Calcium ions do not function as a second messenger for regulatory volume decrease (RVD) in Ehrlich ascites tumor cells.
    • The mechanism of RVD in these cells is independent of a rise in intracellular calcium.
    • While elevated intracellular calcium can induce cell shrinkage, it does so via a pathway distinct from RVD.