Changes in both calcium pool size and morphology of XXXX platelets incubated in various concentrations of calcium ion. Calcium-specific @entity4530 formation on platelet-membrane surface.

@entity1 @entity556 @entity1025 @entity4530 @entity15410 @entity3282 @entity4527 @entity6028 @entity8594 @entity141
In this study, the response of gel-filtered @entity1 platelets to extracellular @entity141 at @entity141 concentrations [ @entity141 ]o of 1-10 mM was investigated. The distribution of @entity141 among various pools was studied using: (1) @entity6028 , to estimate the cytosolic free @entity141 concentration ([ @entity141 ]i); and (2) 45 @entity3282 plus @entity4527 , to quantitate the sizes of the @entity4527 -releasable, @entity4527 -nonreleasable and surface-bound @entity141 pools. The morphological changes were revealed by scanning electron-microscopy (scanning EM), and the effect on @entity556 -stimulated aggregation was examined using an aggregometer. Platelets continuously sequestered @entity141 into both @entity4527 -releasable and @entity4527 -nonreleasable pools to maintain a low [ @entity141 ]i level. The rate of sequestration to the @entity4527 -releasable pool was independent of [ @entity141 ]o, while that of the @entity4527 -nonreleasable pool exhibited first-order kinetics. The cell morphology changed gradually from discoid to the tadpole-like type, and finally to irregular forms. This morphological change correlated with the gradual increase in [ @entity141 ]i. The @entity4527 -nonreleasable pool saturated at about 3000 pmol/10(8) cells. This saturation resulted in a drastic increase in the @entity4527 -releasable pool size, and the cell was lysed concomitantly. The maximum safety capacity of the @entity4527 -releasable pool was estimated to be 1100 pmol/10(8) cells. The contribution of the cellular compartments to these two pool sizes is extensively discussed. The surface-bound pool size also increased continuously. When two different capacities were reached, i.e., 160 and 600 pmol/10(8) cells, the binding rate increased above the initial rate by 7- and 11-fold, respectively. Hence, the surface-binding capacity might be a critical factor which alters the membrane structure and exposes more binding sites. The cell surface appeared to have @entity4530 , after the binding size had reached more than 600 pmol/10(8) cells. Bleb formation resulted in the inhibition of platelet function. Divalent cations, such as @entity1025 , @entity15410 and @entity8594 did not cause @entity4530 formation, which could mean that this formation is a @entity141 -specific phenomenon.
