The aim of the present study was to relate the impairments in
calcium mobilization and/or release to the altered membrane dynamics in platelets from patients with
type 2 diabetes mellitus. Higher expression of
P-selectin (1.4-fold, NS) and the reduction in GPIb alpha expression (by 27.8+/-16.7%, p < 0.0002), as well as the increased fractions of platelet microparticles (p < 0.03), reflected more intensified platelet release reaction in diabetic platelets. Overall, diabetic platelets appeared more vulnerable to stimuli facilitating
calcium mobilization (by 41%, p < 0.01) and less susceptible to preventive effects of the agents hampering
calcium release from intraplatelet storage pools (by 38%, p < 0.01). Both the increased
calcium mobilization from intraplatelet storage pools and higher levels of intracellular free
calcium in the presence of
procaine in diabetic platelets correlated with the reduced platelet
membrane lipid fluidity (resp. pR < 0.03 and pR < 0.015). We conclude that the biophysical state of platelet membrane components in
diabetes mellitus is the crucial determinant of platelet hyperfunction and probably contributes to the intensified
calcium mobilization in diabetic platelets. The depressed preventive effects of
procaine on platelet release reaction and
calcium mobilization in diabetic platelets may result from the primary dislocations and/or distortions of membrane components caused by the diabetic state.