Ca2+ uptake in GH3 cells during hypotonic swelling: the sensory role of stretch-activated ion channels
Chen, Y.; Simasko, S.M.; Niggel, J.; Sigurdson, W.J.; Sachs, F.
American Journal of Physiology 270(6 Pt 1): C1790-C1798
1996
ISSN/ISBN: 0002-9513 PMID: 8764163 Document Number: 463416
Hypotonic cell swelling triggers an increase in intracellular Ca-2+ concentration that is deemed responsible for the subsequent regulated volume decrease in many cells. The understand the mechanisms underlying this increase, we have studied the Ca-2+ sources that contribute to hypotonic cell swelling-induced Ca-2+ increase (HICI) in GH-3 cells. Fura 2 fluorescence of cell populations revealed that extracellular, but not intracellular, stores of Ca-2+ were required. HICI was abolished by nifedipine, a blocker of L-type Ca-2+ channels, and Gd-3+, a nonspecific blocker of stretch-activated channels (SACs), suggesting two components for the Ca-2+ membrane pathway: L-type Ca-2+ channels and SACs. Using HICI as an assay, we found that venom from the spider Grammostola spatulata could block HICI without blocking L-type Ca-2+ channels. The venom did, however, block SAC activity. This suggests that Ca-2+-permeable SACs, rather than L-type Ca-2+ 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.