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Related Experiment Videos

Hypotonically induced calcium increase and regulatory volume decrease in newborn rat cardiomyocytes

K Taouil1, R Giancola, J E Morel

  • 1INSERM U400, Faculté de Médecine, 8, rue du Général Sarrail, F-94010 Créteil, France.

Pflugers Archiv : European Journal of Physiology
|July 31, 1998
PubMed
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Hypotonic cell swelling in newborn rat cardiomyocytes triggers a rapid calcium increase (HICI) dependent on external calcium entry. This HICI is mediated by L-type voltage-activated calcium channels and partially aids regulatory volume decrease.

Area of Science:

  • Cardiology
  • Cell Physiology
  • Calcium Signaling

Background:

  • Cell volume regulation is crucial for cardiomyocyte function.
  • Intracellular calcium concentration ([Ca2+]i) plays a vital role in cardiac cell physiology.
  • The mechanisms linking cell swelling to [Ca2+]i changes are not fully elucidated.

Purpose of the Study:

  • To investigate the effect of hypotonic cell swelling on [Ca2+]i in newborn rat cardiomyocytes.
  • To identify the ion channels and transport mechanisms responsible for the swelling-induced calcium increase (HICI).
  • To explore the role of HICI in the regulatory volume decrease (RVD) process.

Main Methods:

  • Primary culture of newborn rat cardiomyocytes.
  • Induction of hypotonic cell swelling.

Related Experiment Videos

  • Measurement of intracellular calcium concentration ([Ca2+]i) using calcium imaging.
  • Pharmacological inhibition of ion channels and transporters (CPA, ryanodine, Gd3+, diltiazem).
  • Manipulation of ionic gradients (Na+, Ca2+).
  • Assessment of regulatory volume decrease (RVD).

    • Main Results:

    • Hypotonic cell swelling induced a rapid and transient increase in [Ca2+]i (HICI).
    • HICI was dependent on external calcium and was inhibited by diltiazem and membrane predepolarization, suggesting involvement of L-type voltage-activated calcium channels.
    • HICI was not affected by inhibitors of sarcoplasmic Ca2+-ATPase (CPA), calcium-induced calcium release (ryanodine), or stretch-activated cation channels (Gd3+).
    • Neither internal Na+ depletion nor external Na+ omission affected HICI, ruling out Na+-Ca2+ exchange.
    • Removal of external calcium significantly slowed but did not abolish RVD, indicating HICI partially contributes to volume regulation.

    Conclusions:

    • Newborn rat cardiomyocytes exhibit an external calcium-dependent HICI upon hypotonic swelling.
    • L-type voltage-activated calcium channels are implicated in mediating HICI.
    • HICI plays a partial role in the regulatory volume decrease of cardiomyocytes.
    • These findings provide insights into the complex interplay between cell volume, calcium homeostasis, and cell volume regulation in cardiomyocytes.