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The effects of nickel on contraction and membrane current in isolated rat myocytes

S C O'Neill1, M Valdeolmillos, D A Eisner

  • 1Department of Physiology, University College London.

Quarterly Journal of Experimental Physiology (Cambridge, England)
|November 1, 1988
PubMed

Insights

Nickel ions (Ni2+) abolish the tonic tension in myocytes by inhibiting sodium-calcium exchange. This finding supports the role of Na+-Ca2+ exchange in maintaining cardiac contractility.

Area of Science:

  • Cardiology
  • Cellular Physiology
  • Ion Transport

Background:

  • Depolarization of cardiac myocytes can induce sustained tension.
  • The mechanisms regulating tonic tension in myocytes are not fully understood.
  • Sodium-calcium exchange (Na+-Ca2+ exchange) is a key regulator of intracellular calcium.

Purpose of the Study:

  • To investigate the role of Na+-Ca2+ exchange in the maintained tonic tension of isolated myocytes.
  • To determine the effect of Ni2+ on tonic contraction and associated ionic currents.

Main Methods:

  • Isolated myocytes were subjected to prolonged depolarization.
  • The effects of 5 mM Ni2+ on tonic tension development and relaxation were assessed.
  • Ionic currents and intracellular calcium ([Ca2+]i) changes were measured.

Main Results:

  • A maintained, tonic component of tension was observed following depolarization.
  • 5 mM Ni2+ abolished this tonic tension and prevented relaxation once developed.
  • Ni2+ abolished the transient inward current without affecting the underlying [Ca2+]i changes.

Conclusions:

  • The results strongly support the hypothesis that Ni2+ inhibits Na+-Ca2+ exchange in cardiac myocytes.
  • Inhibition of Na+-Ca2+ exchange by Ni2+ prevents the development and relaxation of tonic contraction.
  • Na+-Ca2+ exchange plays a critical role in regulating sustained myocyte tension.

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