Year: 1981
Type: conference-paper
Abstract: Ticlopidin (T) is a potent inhibitor of platelet aggregation which enhanced the platelet sensitivity to anti-aggregating prostaglandins such as PGE1. The goal of this study was to examine the site of action of T in the rat platelets after in vivo administration, in respect to the PGE1 mechanism of action. Male adult Wistar rats were orally administered at the dose of 200 mg/kg, 20 and h hours before blood collection. The binding of (3H)-PGE1 to platelets from controls and treated rats was determined by filtration technique. The c AMP formation was measured by protein binding assay in aspirin-washed platelet suspension or in lysate after stimulation by PGE1, adenosine or NaF. Since potentiation of PGE1 by T occured in aspirin-washed platelets, it is independent of the ability of the cells to synthesise prostaglandins. On the other hand, PGE1-receptor binding is not affected by T treatment and potentiation of PGE1 effect is not specific. Moreover, basal adenylate cyclase activity is increased in platelet particulate fraction of treated rats, but NaF stimulation is not enhanced. These results suggest that T activates the adenylate cyclase systems by an action on the coupler subunit of the enzyme just as guanosine triphosphate does.
Source: Thrombosis and Haemostasis
Authors: C Bonne, B Martin, F Regnault
Institution: Inserm
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2884979920