Regulation of agonist-evoked [Ca2+](i) oscillation by intracellular Ca2+ and Ba2+ in AR42J cells

B. X. Zhang, H. Zhao, P. A. Loessberg, S. Muallem

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16 Scopus citations


Measurements of intracellular Ca2+ ([Ca2+](i)) and intracellular Ba2+ ([Ba2+](i)) in single AR42J cells were used to evaluate the effect of [Ca2+](i) and [Ba2+](i) on agonist-evoked [Ca2+](i) oscillations. Variations in [Ca2+](i) and [Ba2+](i) were imposed by gradual activation of entry through voltage-activated Ca2+ channels (VACC) present in the plasma membrane of these cells. Activation by high K+ was followed by partial inactivation of the channels and stabilization of [Ca2+](i) at a new steady-state level depending on the extent of depolarization. Activation by BAY K 8644 was followed by complete inactivation and return of [Ca2+](i) to resting levels. Ba2+ activated the channels and entered the cells but could not be removed from the cytosol by cellular Ca2+ pumps. The use of channel blockers and the ability to increase [Ca2+](i) and [Ba2+](i) by channel activation during [Ca2+](i) oscillations showed that VACC do not contribute to or are activated during agonist-stimulated Ca2+ oscillation in this cell type. Graded activation of VACC showed that an increase in [Ca2+](i) between the spikes to below 200 nM increased the frequency of the oscillation. Further increase in [Ca2+](i) caused gradual reduction in the frequency. At [Ca2+](i) above 500 nM, [Ca2+](i) oscillations were inhibited. The inhibitory but not the stimulatory effects of [Ca2+](i) on the oscillations can be mimicked by [Ba2+](i). These observations suggest that [Ca2+](i) levels between the spikes play an important role in regulating the oscillations.

Original languageEnglish (US)
Pages (from-to)C1125-C1133
JournalAmerican Journal of Physiology - Cell Physiology
Issue number5 31-5
StatePublished - 1992


  • intracellular barium
  • intracellular calcium
  • voltage-activated calcium channels

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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