This preclinical study supports the hypothesis that increased intracellular cAMP levels in human platelets inhibit platelet aggregation.
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Supports cAMP-mediated platelet inhibition in animal models; leaves open translation to human antithrombotic strategies.
Evidence which bears on the hypothesis that agents that increase platelet cyclic adenosine 3',5' monophosphate (cAMP) tend to inhibit platelet aggregation, whereas agents whose action is to induce or augment platelet aggregation are associated with a decrease in platelet content of this cyclic nucleotide is reviewed. Using radiolabeled cAMP in incubation with various agents, it was found that caffeine, colagen, thrombin, prostaglandins E1 and E2, and phosphodiesterase inhibitors are all agents that increase platelet cAMP and inhibit platelet aggregation.
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Salzman et al. (1972) studied this question.
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