AJP - Gastrointestinal and Liver Physiology, Vol 238, Issue 4 338-G348, Copyright © 1980 by American Physiological Society
Effect of atropine, ouabain, antimycin A, and A23187 on "trigger Ca2+ pool" in exocrine pancreas
H. Stolze and I. Schulz
45Ca2+ fluxes have been analyzed in dispersed acinar cells prepared from
rat pancreas. Sudden addition of carbamylcholine (CCh) to 45Ca2+-preloaded
acinar cells at quasi-steady state for 45Ca2+ resulted in a quick 45Ca2+
release followed by a slower 45Ca2+ reuptake with net accumulation of
45Ca2+. Subsequent sudden addition of atropine caused a further transient
increase in cellular 45Ca2+ followed by a slow decrease to a steady-state
value. 45Ca2+ release could not be evoked a second time by pancreozymin
when prestimulated with CCh. However, if CCh stimulation was abolished by
an interposed step of atropine, restimulation by
cholecystokinin-pancreozymin was possible. Addition of A23187 or antimycin
A to cells induced a fast decrease in cellular 45Ca2+. This effect was not
additive to the CCh effect. In ouabain-pretreated cells, the CCh-induced
sudden loss of cellular 45Ca2+ was blocked by 60%. The following slow
reuptake of 45Ca2+ was blocked completely. Subsequent addition of atropine
caused a fast uptake of cellular 45Ca2+ with no secondary decline. The data
are consistent with the following model: acetylcholine releases Ca2+ from a
cellular "trigger pool" into the cytosol located in or near the cell
membrane. Then Ca2+ is extruded from the cell via Ca2+ pumps partly by a
Na+-dependent Ca2+ transport system (quick phase of 45Ca2+ release).
Subsequently, due to increased Ca2+ permeability of the plasma membrane as
induced by acetylcholine, Ca2+ influx occurs and Ca2+ is taken up from the
cytosol into intracellular Ca2+ pools (slow 45Ca2+ reuptake phase).
Atropine causes refilling of the trigger Ca2+ pool and return of the
increased Ca2+ permeability of the plasma membrane back to the unstimulated
state.
