AJP - Gastrointestinal and Liver Physiology, Vol 250, Issue 3 280-G286, Copyright © 1986 by American Physiological Society
Source of activator calcium in isolated guinea pig and human gastric muscle cells
K. N. Bitar, G. M. Burgess, J. W. Putney Jr and G. M. Makhlouf
The source of Ca2+ responsible for contraction was examined in suspensions
of smooth muscle cells and in perfused single muscle cells from guinea pig
and human stomach. In both preparations removal of Ca2+ from the medium or
addition of the Ca2+ channel blocker methoxyverapamil had no effect on the
contractile response to various agonists, including cholecystokinin
octapeptide (CCK-8) and acetylcholine, but inhibited the response to high
extracellular K+ by 76-82%. Repeated stimulation of guinea pig or human
single muscle cells in Ca2+-free medium, or in the presence of
methoxyverapamil caused a progressive decrease and eventual abolition of
contractile response; response was restored on restitution of Ca2+ to the
medium or elimination of methoxyverapamil. Measurement of 45Ca2+ content in
guinea pig muscle cells showed that CCK-8 had no effect on the rate of Ca2+
influx but increased the rate of Ca2+ efflux transiently by sixfold. Net
peak efflux coincided with the time of peak contraction and was
stoichiometrically related to the degree of contraction. Equipotent,
maximally effective contractile doses of CCK-8, acetylcholine, and
methionine-enkephalin caused equivalent degrees of net Ca2+ efflux. The
results indicate that contractile agonists cause release of Ca2+ from a
depletable intracellular store in gastric muscle cells. The release is
accompanied by a dose-dependent increase in Ca2+ efflux and is capable of
sustaining an initial maximal contraction. Repeated contractile activity
requires influx of Ca2+ from extracellular sources.
