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Related Experiment Videos

Intracellular Ca2+ release and Ca2+ influx during regulatory volume decrease in IMCD cells

H Tinel1, F Wehner, H Sauer

  • 1Max Planck Institute for Molecular Physiology, Dortmund, Germany.

The American Journal of Physiology
|July 1, 1994
PubMed
Summary
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Hypotonic stress causes inner medullary collecting duct (IMCD) cells to swell and release intracellular calcium, which is essential for regulatory volume decrease (RVD). Inhibiting calcium release blocks this RVD response.

Area of Science:

  • Cell Physiology
  • Renal Physiology
  • Calcium Signaling

Background:

  • Inner medullary collecting duct (IMCD) cells are crucial for renal water and solute balance.
  • Cell volume regulation is vital for cellular function, particularly under osmotic stress.
  • Calcium ions play a significant role in various cellular processes, including volume regulation.

Purpose of the Study:

  • To investigate the role of cytosolic calcium concentration ([Ca2+]i) in IMCD cell volume changes under hypotonic stress.
  • To elucidate the mechanisms of calcium release and entry during regulatory volume decrease (RVD) in IMCD cells.

Main Methods:

  • Confocal laser scanning microscopy to monitor IMCD cell volume.
  • Fura 2 fluorescence to measure cytosolic calcium concentration ([Ca2+]i).

Related Experiment Videos

  • Use of specific inhibitors (TMB-8, caffeine) and manganese (Mn2+) influx assay to study calcium dynamics.

    • Main Results:

    • Hypotonic stress induced IMCD cell swelling and a significant increase in [Ca2+]i.
    • Regulatory volume decrease (RVD) was impaired when extracellular calcium was low or when intracellular calcium release was inhibited.
    • Intracellular calcium release preceded calcium influx, and inhibiting release reduced influx, suggesting intracellular calcium triggers plasma membrane calcium channel activation.

    Conclusions:

    • Cytosolic calcium increase, originating from intracellular stores, is essential for initiating RVD in IMCD cells under hypotonic conditions.
    • The findings highlight a critical role for intracellular calcium signaling in mediating the cellular response to osmotic challenges in the kidney.