calcimycin and 5-6-dihydroprostacyclin

calcimycin has been researched along with 5-6-dihydroprostacyclin* in 1 studies

Other Studies

1 other study(ies) available for calcimycin and 5-6-dihydroprostacyclin

Article	Year
Decrease of platelet aggregation and spreading via inhibition of the cAMP phosphodiesterase by trapidil. FEBS letters, 1984, Jul-09, Volume: 172, Issue:2 Trapidil (N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine ) inhibits platelet spreading and aggregation induced by arachidonic acid (AA), a stable analogue of prostaglandin (PG) endoperoxides (U46619), ADP, and low concentrations of thrombin, but not by A23187 and high concentrations of thrombin. Trapidil does not affect platelet adenylate cyclase but inhibits the cAMP PDE by approx. 50%. PDE inhibition proceeds via a competitive mechanism (Ki = 0.52 mM) and is not mediated by calmodulin inhibition. Trapidil does not change the platelet basal cAMP level but potentiates an increase of cAMP induced by the stable prostacyclin analogue (6 beta-PGI1). These results suggest that trapidil antiplatelet effects may be due to the inhibition of platelet PDE. Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; 3',5'-Cyclic-AMP Phosphodiesterases; Adenosine Diphosphate; Arachidonic Acid; Arachidonic Acids; Calcimycin; Cyclic AMP; Epoprostenol; Humans; Platelet Adhesiveness; Platelet Aggregation; Prostaglandin Endoperoxides, Synthetic; Pyrimidines; Theophylline; Thrombin; Trapidil	1984

Article

Year

Decrease of platelet aggregation and spreading via inhibition of the cAMP phosphodiesterase by trapidil.

FEBS letters, 1984, Jul-09, Volume: 172, Issue:2

Trapidil (N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine ) inhibits platelet spreading and aggregation induced by arachidonic acid (AA), a stable analogue of prostaglandin (PG) endoperoxides (U46619), ADP, and low concentrations of thrombin, but not by A23187 and high concentrations of thrombin. Trapidil does not affect platelet adenylate cyclase but inhibits the cAMP PDE by approx. 50%. PDE inhibition proceeds via a competitive mechanism (Ki = 0.52 mM) and is not mediated by calmodulin inhibition. Trapidil does not change the platelet basal cAMP level but potentiates an increase of cAMP induced by the stable prostacyclin analogue (6 beta-PGI1). These results suggest that trapidil antiplatelet effects may be due to the inhibition of platelet PDE.

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; 3',5'-Cyclic-AMP Phosphodiesterases; Adenosine Diphosphate; Arachidonic Acid; Arachidonic Acids; Calcimycin; Cyclic AMP; Epoprostenol; Humans; Platelet Adhesiveness; Platelet Aggregation; Prostaglandin Endoperoxides, Synthetic; Pyrimidines; Theophylline; Thrombin; Trapidil

1984