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Zebrafish yolk sac microinjection of thalidomide for assessment of developmental toxicology

Toxicological Evaluation of SiO2 Nanoparticles by Zebrafish Embryo Toxicity Test

Increased susceptibility to oxidative stress-induced toxicological evaluation by genetically modified nrf2a-deficient zebrafish.

EGF receptor kinase suppresses ciliogenesis through activation of USP8 deubiquitinase

Chemokines protect vascular smooth muscle cells from cell death induced by cyclic mechanical stretch.

tEffects of cilostazol, a selective cAMP phosphodiesterase inhibitor on the contraction of vascular smooth muscle..


Tanaka T, Ishikawa T, Hagiwara M, Onoda K, Itoh H, Hidaka H.
Pharmacology. 1988;36(5):313-20.


The effects of cilostazol (OPC-13013, 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)-quin olinone) on cyclic nucleotide metabolism and Ca2+-induced contraction of intact and skinned rabbit arterial smooth muscles were investigated. The concentrations of cilostazol producing 50% inhibition of cyclic adenosine monophosphate phosphodiesterase and Ca2+-dependent cyclic nucleotide phosphodiesterase were 0.4 microM and above 100 microM, respectively. This compound has no significant effect on adenylate cyclase in concentrations of up to 100 microM. Addition of cilostazol increased significantly the cAMP content without significant effect on cyclic guanosine monophosphate level of rabbit thoracic aorta in the presence of forskolin. Moreover, the ED50 value of cilostazol in relaxation of rabbit mesenteric arterial strips was decreased selectively by addition of 0.01 microM forskolin, which alone at this concentration has no effect on vascular contraction. Cilostazol of up to 30 microM did not suppress the Ca2+-induced contraction of the chemically skinned rabbit mesenteric artery. Therefore, cilostazol may produce the relaxation of intact vascular smooth muscle by its inhibition of cyclic adenosine monophosphate hydrolysis.