Last update:
02-Nov-2000

Arch Hellen Med, 17(2), March-April 2000, 157-160

BRIEF REVIEW

The effect of ADP on blood platelet morphology
and the role of thienopyridines

ADP is a weak, natural platelet agonist. Its mechanism of action is not completely understood, but ultimately it acts via the GPIIb-IIIa complex where the fibrinogen receptor resides at the platelet surface. ADP plays two roles which cooperate to produce platelet activation. ADP in low concentrations (0.1–0.5 μM) produces a change in shape from a discoid to a spherical form and then to an echinoid form (with the production of filopods), followed by reversible aggregation. ADP in higher concentrations (2.5–5.0 μM) produces release of dense, α-storage granular contents and secondary, irreversible aggregation. The thienopyridines, ticlopidine and clopidogrel, inhibit platelet adhesion to the vascular subendothelium. The ADP-induced change in shape is not inhibited by treatment with thienopyridines, but they inhibit ADP-induced α-granule secretion. The granules contain adhesive proteins, such as fibrinogen, mitogenic factors, P-selectin and others. Also, thienopyridines inhibit the ADP-induced exposure of the fibrinogen binding site (receptor), which resides on the GPIIb-IIIa complex. Overall, thienopyridines lead to inhibition of secondary, irreversible platelet aggregation and they are effective inhibitors of shear stress-induced platelet activation.

Key words: ADP, Morphology and blood platelet, Thienopyridines.