AJP - Cell Physiology, Vol 267, Issue 5 C1435-C1441, Copyright © 1994 by American Physiological Society
Calcium-activated sodium and chloride fluxes modulate platelet volume: role of Ca2+ stores
B. P. Fine, E. S. Marques and K. A. Hansen
Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103.
An increase in cytosolic ionized Ca2+ concentration ([Ca2+]i) initiates
volume changes in various types of cells. In response to increases in
[Ca2+]i most cell types contract by efflux of K+ and Cl-, whereas platelets
expand in response to rises in [Ca2+]i. This study examined the importance
of the source of Ca2+, the flux of ions responsible for the volume change,
and the role of Ca(2+)-dependent protein kinases in regulating these ionic
fluxes. The baseline platelet volume was independent of extracellular Ca2+
but when stimulated by the Ca2+ ionophore A-23187 (50 nM) the volume
increased in both the presence and absence of extracellular Ca2+ (1.18 +/-
0.08 vs. 0.83 +/- 0.06 fl, respectively). The increased volume was caused
by the gain of Na+ and Cl-. Na+ entered through both conductive and
nonconductive (Na+/H+ exchange) pathways, whereas the influx of Cl- was
conductive and inhibited by the Cl- channel blocker
4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. The Ca(2+)-induced volume
change was blocked by both calmodulin and protein kinase inhibitors. Thus
the activation of Ca(2+)-dependent protein kinases promotes platelet
swelling by stimulating Na+ and Cl- influx.
