Abstract

The rate of ADP-induced aggregation of platelets was increased markedly by 1-epinephrine or norepinephrine. Naphazoline, N-methyl epinephrine or d-epinephrine also produced significant increases in rate. In contrast, other α- or β-receptor agonists or indirectly acting agents (d-norepinephrine, phenylephrine, synephrine, metanephrine, tyramine, dopamine, isoproterenol, salbutamol) did not accelerate aggregation. None of the sympathomimetics tested was able to induce aggregation when used alone. Important structural requirements of epinephrine for acceleration of aggregation were R-configuration, a β-hydroxyl group, a catechol moiety, and the absence of large N-alkyl groups. The potentiating effect of epinephrine was blocked equally well by d- or 1-phenoxybenzamine and by propranolol; however, the latter compound did so at concentrations which inhibited ADP aggregation alone. These results with various agonists and antagonists indicate that the receptor involved in catecholamine acceleration of ADP-aggregation does not have all the usual characteristics of either the α- or β-adrenergic receptor.

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