Influence of Adrenergic Receptor Blockade on Aspirin-induced Inhibition of Platelet Function.
Studies from our laboratory have demonstrated that epinephrine via alpha(2)-adrenoreceptor modulation can restore the sensitivity of aspirin-treated platelets to the action of agonists independent of secretion of granule contents or synthesis of prostanoids. The present study has evaluated the effects of full strength aspirin (take on alternate days) and low dose aspirin (taken daily) and sought to determine whether agents which antagonise alpha or beta adrenergic receptors can prevent the corrective influence of epinephrine on aspirin-treated platelets. Adult volunteers were given 325 mg aspirin every other day or 80 mg aspirin daily. After confirming the inhibitory effect of aspirin, these individuals were given yohimbine (5 mg), atenolol (100 mg), verapamil (160 mg) or ethanol (white wine 8 oz). Two hours later, blood was drawn for platelet studies. Cells exposed to aspirin did not aggregate when stirred with arachidonate (0.45 mM) or epinephrine (5 M) alone. Addition of epinephrine to aspirin treated platelets restored the sensitivity to the action of arachidonate and resulted in irreversible aggregation. Ethanol and verapamil at the concentrations tested did not potentiate the action of aspirin. Ingestion of yohimbine, an alpha(2)-adrenergic antagonist, or atenolol, a beta blocker, prevented the corrective influence of epinephrine on aspirin-treated refractory platelets. Results suggest that alpha and beta blockers may serve a useful role in reinforcing the antithrombotic influence of aspirin in vivo.
Department of Laboratory Medicine and Pathology, University of Minnesota Health Sciences Center, Box 198 UMHC, 420 Delaware Street SE, University of Minnesota, Minneapolis, 55455, USA.
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