Platelet β‐adrenoceptors

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Abstract
1 Inhibition by isoprenaline of the aggregatory response of human and rat platelets induced by various excitatory agonists is blocked by β2-adrenoceptor antagonists, β1-Adrenoceptor antagonists are ineffective. 2 β2-Adrenoceptor agonists cause inhibition of the response of human platelets to various excitatory agonists. The maximal extent of inhibition is less than that observed for isoprenaline. β1-Adrenoceptor agonists fail to cause detectable inhibition of this response. Neither β1 nor β2-adrenoceptor agonists cause inhibition of the response of rat platelets to excitatory agonists. Only β2-adrenoceptor agonists block the inhibitory response to isoprenaline. 3 The extent of inhibition by isoprenaline is a function of the excitatory agonist used and in human platelets is correlated with the ability of that agonist to suppress elevated platelet cyclic adenosine 3′,5′-monophosphate (cyclic AMP) levels. 4 Inhibition by isoprenaline is prevented in the presence of an inhibitor of adenylate cyclase. 5 Isoprenaline increases platelet cyclic AMP levels with an EC50 similar to that required to observe inhibition of the aggregatory response. 6 These data indicate that human platelets carry β2-adrenoceptors whose occupancy causes inhibition of the response to excitatory agonists as a consequence of elevation of platelet cyclic AMP. The β-adrenoceptor present on rat platelets also appears to be of the β2-subtype.