Key result
Prostaglandin E analogues, particularly sulprostone, potentiated platelet aggregation and inhibited adenylate cyclase in human platelets, likely mediated by an 'EP3-like' receptor.
Population
Platelet-rich plasma and washed platelet suspensions from human donors
Design
Preclinical
Authors
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May indicate pro-aggregatory risk with PGE analogues; hypothesis-generating for EP3-like receptor as antithrombotic target.
PGE analogues potentiate human platelet aggregation through an EP3-like receptor, which is linked to the inhibition of adenylate cyclase.
Matthews et al. (1993) studied this question. Prostaglandin E analogues (e.g., sulprostone) was evaluated on Platelet aggregation potentiation and cyclic AMP inhibition. Prostaglandin E analogues, particularly sulprostone, potentiated platelet aggregation and inhibited adenylate cyclase in human platelets, likely mediated by an 'EP3-like' receptor.
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