Question

What is the mechanism of action accounting for dipyridamole's use as an anti-platelet agent?

a) Inhibition of thromboxane synthesis
b) Inhibition of ADP-induced platelet aggregation
c) Prevention of fibrinogen binding
d) Activation of glycoprotein IIb/IIIa

Answer 1

The mechanism of action for dipyridamole involves inhibiting phosphodiesterase, leading to increased cAMP in platelets which prevents aggregation, and increasing adenosine levels that further inhibit platelet function.

Step-by-step explanation:

The mechanism of action for dipyridamole as an anti-platelet agent is its ability to inhibit phosphodiesterase, which leads to an increase in cyclic adenosine monophosphate (cAMP) within platelets. This accumulation of cAMP inhibits platelet aggregation by decreasing calcium concentration in the platelets, thus preventing platelets from sticking together and forming a clot. Dipyridamole also blocks the reuptake of adenosine into erythrocytes and endothelial cells, leading to increased adenosine levels, which in turn, can inhibit platelet aggregation via A2 adenosine receptors. Dipyridamole's anti-platelet effect is distinct from the action of aspirin, which irreversibly inhibits cyclooxygenase-1 (COX-1), thereby blocking the formation of thromboxane A2, a potent promoter of platelet aggregation.