Ca2+ uptake in gh3 cells during hypotonic swelling; evidence for
the sensory role of stretch activated ion channels.
Chen, Ye, Steven M. Simasko, Jeffrey Niggel Wade, J. Sigurdson, and
Frederick Sachs.
Department of Biophysical Sciences, SUNY at Buffalo, Buffalo, NY
14214
APStracts 2:0443C, 1995.
Hypotonic cell swelling triggers an increase in [Ca2+]i which is
deemed responsible for the subsequent regulated volume decrease in
many cells. To understand the mechanisms underlying this increase, we
have studied the Ca2+ sources that contribute to HICI (hypotonic cell
swelling induced Ca2+ increase) in GH3 cells. Fura-2 fluorescence of
cell populations revealed that extracellular, but not intracellular
stores, of Ca2+, were required. HICI was abolished by nifedipine, a
blocker of L-type Ca2+ channels, and Gd3+, a non-specific blocker of
stretch-activated channels (SACs), suggesting two components for the
Ca2+ membrane pathway: L-type Ca2+ channels and SACs. Using HICI as
an assay, we found that venom from the spider Grammostola spatulata
could block HICI without blocking L-type Ca2+ channels. The venom
did, however, block SAC activity. This suggests that Ca2+ permeable
SACs, rather than L-type Ca2+ channels, are the sensing elements for
HICI. These results support the model for volume regulation in which
SACs, activated by an increase of the membrane tension during
hypotonic cell swelling, trigger HICI leading to a volume decrease.
Received 20 June 1995; accepted in final form 1 December 1995.
APS Manuscript Number C356-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95