Volume‐regulating behavior of human platelets

Publisher Website
Google Scholar
Abstract
Human platelets exposed to hypotonic media undergo an initial swelling followed by shrinking (regulatory volume decrease [RVD]). If the RVD is blocked, the degree of swelling is in accord with osmotic behavior. The cells could swell at least threefold without significant lysis. Two methods were used to follow the volume changes, electronic sizing and turbidometery. Changes in shape produced only limited contribution to the measurements. The RVD was very rapid, essentially complete in 2 to 8 minutes, with a rate proportional to the degree of initial cell swelling. RVD involved a loss of KCI via volume‐activated conductive permeability pathways for K+ and anions, presumably Cl −. In media containing > 50 mM KCI, the shrinking was inhibited and with higher concentrations was reversed (secondary swelling), suggesting that it is driven by the net gradient of K+ plus Cl−. The K+pathway was specific for Rb+ and K+ compared to Li+ and Na+. The Cl− pathway accepted NO3− and SCN− but not citrate or SO2‐4. In isotonic medium, the permeability of platelets to Cl− appeared to be low compared to that of K+. After hypotonic swelling both permeabilities were increased, but the Cl− permeability exceeded that of K+. The Cl− conductive pathway remained open as long as the cells were swollen. RVD was incomplete unless amiloride, an inhibitor of Na+ /H+ exchange, was present or unless Na+ was replaced by an impermeant cation. In addition, acidification of the cytoplasm occurred upon cell swelling. This reduction in pHi appeared to activate Na+/ H+ exchange, with a resultant uptake of Na+ and reduction in the rate and amount of shrinking. Like other cells, platelets responded to hypertonic shrinking with activation of Na+/H+ exchange, but regulatory volume increase was not detectable.