Potent effects of novel anti-platelet aggregatory cilostamide analogues on recombinant cyclic nucleotide phosphodiesterase isozyme activity

Cilostazol Reduces Target Lesion Revascularization After Percutaneous Transluminal Angioplasty in the Femoropopliteal Artery

“…[28][29][30] In addition, inhibition of vascular smooth muscle cell proliferation has also been reported. 11,12 Inhibition of smooth muscle cell proliferation and the vasodilatory effects are unique features of cilostazol that other antiplatelet drugs do not possess and may contribute to the reduction in TLR after PTA in the clinical setting.…”

The Phosphodiesterase 3 Inhibitor Cilostazol Dilates Large Cerebral Arteries in Humans Without Affecting Regional Cerebral Blood Flow

“…Furthermore, in 38.1 ± 5.6 38.7 ± 2.4 113 ± 13 110 ± 13 63 ± 6 62 ± 7 59 ± 12 66 ± 13 120.00 37.8 ± 5.3 37.9 ± 3.5 112 ± 12 115 ± 9 65 ± 7 63 ± 7 59 ± 10 66 ± 12 135.00 38.0 ± 5.6 38.3 ± 3.0 111 ± 12 112 ± 13 64 ± 9 62 ± 7 55 ± 8 63 ± 12 150.00 37.9 ± 5.1 38.5 ± 3.3 112 ± 10 112 ± 10 65 ± 7 60 ± 7 57 ± 11 62 ± 13 165.00 37.8 ± 5.3 37.4 ± 3.6 111 ± 13 111 ± 8 63 ± 6 62 ± 6 56 ± 10 67 ± 15 180.00 36.8 ± 5.4 37.3 ± 3.7 114 ± 12 111 ± 9 64 ± 7 61 ± 10 60 ± 10 63 ± 12 195.00 38.0 ± 4.7 38.4 ± 2.8 112 ± 12 113 ± 10 66 ± 9 61 ± 8 55 ± 11 65 ± 13 210.00 37.7 ± 5.1 38.1 ± 2.4 115 ± 12 112 ± 10 64 ± 8 64 ± 11 60 ± 12 66 ± 13 225.00 37.3 ± 4.8 37.3 ± 2.8 114 ± 13 115 ± 10 67 ± 8 64 ± 8 57 ± 11 66 ± 14 240.00 36.1 ± 5.2 36.4 ± 3.1 117 ± 11 119 ± 9 69 ± 8 66 ± 7 60 ± 11 49 ± 17 high concentrations (10 mol/L), cilostazol inhibits recombinant human PDE5, one of the major cyclic GMP hydrolyzing enzymes (Sudo et al, 2000), and correspondingly increases cyclic CMP in a cyclic nucleotide assay (Birk et al, 2004a). However, PDE5 inhibition does not appear to play any significant role in the functional relaxant response to cilostazol (Birk et al, 2004a), and the highly potent and selective PDE5 inhibitor sildenafil does not dilate the MCA or increase CBF in a similar experimental setup as the present (Kruuse et al, 2003;Kruuse et al, 2002).…”

Differential Effect of Phosphodiesterase-3 Inhibitors on Sympathetic Hyperinnervation in Healed Rat Infarcts

“…41 However, PDE-5 inhibition does not appear to play a significant role in the NGF expression associated with cilostazol because cilostazol as a PDE-5 antagonist requires a higher therapeutic concentration (10 μmol/L) than reported in this study. 40 Third, cilostazol appears to possess an additional effect that does not require inhibition of PDEs. 42 Cilostazol may directly inhibit secretion of catecholamine through its blocking action on Ca 2+ movement in adrenal chromaffin cells.…”

“…39 Thus, it is possible, at least in theory, that the greater selectivity of cilostazol for PDE-3 may help prevent cardiac arrhythmias. Second, cilostazol has been shown to inhibit recombinant human PDE-5, a major cGMP hydrolyzing enzyme, 40 and correspondingly increases cGMP. cGMP has been shown to downregulate NGF expression.…”