Do human platelets have opiate receptors?

Abstract

In their study of prostaglandin E₁ (PGE₁)-sensitive adenylate cyclase (AC) in rat brain homogenates, Collier and Roy¹ claimed that the activity of this enzyme is inhibited by opiates. They also proposed that opiates exert their analgesic and allied effects by inhibiting AC of neurones that are normally stimulated by E prostaglandins². Studies using neuroblastoma × glioma hybrid cells^3,4 supported this hypothesis. However, subsequent studies with the mammalian brain^5,6 and rat brain tissue slices^7,8 yielded conflicting results. PGE₁, also inhibits platelet aggregation⁹, probably through activation of platelet AC¹⁰. Gryglewski et al.¹¹ showed that morphine inhibits the anti-aggregating effect of PGE₁ on ADP- and adrenaline-induced platelet aggregation, and suggested that the inhibition by morphine is mediated through platelet AC activity. We report here our attempts to reproduce the results of Gryglewski et al. and our examination of the effect of morphine on PGE₁-sensitive AC activity in platelet lysates and on PGE₁-induced accumulation of cyclic AMP in intact platelets. The possible existence of opiate receptors in platelets was also assesed by direct binding studies with ³H-etorphine. In contrast to Gryglewski et al.¹¹, we could not detect any effect of opiates on the aggregation of human platelets, nor did we find any other evidence supporting the presence of opiate receptors in these cells. Thus we conclude that the presence of opiate receptors in human platelets is unlikely.