Systemic: Cilostazol and its active metabolites inhibit phosphodiesterase activity and suppress degradation of cyclic adenosine monophosphate (cAMP) resulting in an increase in cAMP in platelets and blood vessels. It reversibly inhibits platelet aggregation induced by various stimuli, including thrombin, adenosine diphosphate (ADP), collagen, arachidonic acid, epinephrine, and shear stress.[9] Cilostazol produces non-homogenous vasodilation, with greater dilation in femoral beds than in vertebral, carotic, or superior mesenteric arteries, but without effect in renal arteries.[9]