Key result
Therapeutically relevant concentrations of dipyridamole amplified NO/cGMP-mediated VASP phosphorylation in human platelets, enhancing platelet inhibition ex vivo.
Why the study?
Does dipyridamole enhance NO/cGMP-mediated VASP phosphorylation and signaling in human platelets?
Population
Human platelets (in vitro) and healthy volunteers (ex vivo)
Comparison
Dipyridamole vs Vehicle or baseline (absence of dipyridamole)
Design
Preclinical
Follow-up
3 hours
Authors
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Supports mechanistic role of dipyridamole in NO-mediated platelet inhibition; leaves open whether this improves stroke outcomes.
Does dipyridamole enhance NO/cGMP-mediated VASP phosphorylation and signaling in human platelets?
Dipyridamole enhances platelet inhibition by amplifying NO/cGMP-mediated signaling, providing a mechanistic explanation for its clinical efficacy in stroke prevention.
Aktas et al. (2003) studied this question. Therapeutically relevant concentrations of dipyridamole amplified NO/cGMP-mediated VASP phosphorylation in human platelets, enhancing platelet inhibition ex vivo.
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