The ability of epinephrine to expose platelet fibrinogen receptors independent of released ADP was assessed using aspirin-treated, gel-filtered platelets. Similar to ADP-induced aggregation, platelet aggregation in response to epinephrine was accompanied by fibrinogen binding. Ten micromolar epinephrine induced a maximum number of platelet fibrinogen receptors in the absence of significant 14C-serotonin release. As indicated by Scatchard analysis, receptors exposed by both epinephrine and ADP had similar affinities for fibrinogen, but epinephrine induced approximately 30% fewer receptors than did ADP. This appears to correlate with the lesser degree of primary aggregation observed with this agent. Studies using phentolamine, a specific alpha-adrenergic antagonist, apyrase, or creatine phosphate/creatine kinase indicate that the exposure of platelet fibrinogen receptors by epinephrine was specific for platelet alpha-adrenergic receptor stimulation and was not the result of released ADP.

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