AJP - Cell Physiology, Vol 262, Issue 5 C1125-C1133, Copyright © 1992 by American Physiological Society
Regulation of agonist-evoked [Ca2+]i oscillation by intracellular Ca2+ and Ba2+ in AR42J cells
B. X. Zhang, H. Zhao, P. A. Loessberg and S. Muallem
Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75235.
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 of 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.
