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β-Blocking Agents and Platelet Aggregation

M. Rubegni; D. Provvedi; P. G. Bellini
JAMA. 1974;228(4):462. doi:10.1001/jama.1974.03230290018012.
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To the Editor.—  There is general agreement that substances that inhibit platelet aggregation tend to be associated with a rise in platelet cyclic adenosine monophosphate (cAMP), and those that stimulate platelet-clumping with the reverse.1Epinephrine reduces platelet cAMP by inhibition of adenyl cyclase. Like epinephrine-induced platelet aggregation, this phenomenon is an α-adrenergic effect, being subject to blockade by phentolamine.2Hampton et al3 discovered that propranolol inhibited noradrenaline-induced platelet aggregation. Propranolol proved also to be a powerful inhibitor of adenosine diphosphate (ADP)-induced aggregation and of potentiating effect of epinephrine on the second phase of ADP-induced aggregation.4 It seems that this effect would be not related to β-blocking activity but to a stabilizing action on biological membranes like imipramine and related compounds.5In regard to its cardiac effects, propranolol appears to have a more evident activity on the inhibition of platelet aggregation.


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