Regulation of platelet function by catecholamines in the cerebral vasculature of the rabbit

1 In-111-labelled platelets were monitored continuously in the cerebral and pulmonary vascular beds of anaesthetized rabbits. Dopamine can, depending upon the concentration, either potentiate or inhibit thrombin-induced plate let accumulation in the cerebral vasculature of rabbits by unknown mechanis ms. The effects of specific adrenergic and dopaminergic receptor antagonist s were tested upon dopamine's actions on intracarotid (i.c.) thrombin-induc ed (80 u kg(-1)) platelet accumulation in the cerebral vasculature. The eff ect of adrenaline on the response to thrombin in this vascular bed was also investigated. 2 Thrombin-induced platelet accumulation was significantly (P<0.01) potenti ated by dopamine (100 mu g kg(-1) min(-1), i.c.) and this effect was signif icantly inhibited by infusion of the alpha-adrenoceptor antagonist, phentol amine. 3 A higher dose of dopamine (2 mg kg(-1) min(-1), i.c.) inhibited thrombin- induced platelet accumulation. The beta-adrenoceptor antagonist, propranolo l, did not significantly alter this inhibitory effect whereas it was abolis hed by the dopamine D1 selective antagonist, SCH23390. 4 Adrenaline (when administered i.c. by bolus injection or infusion) had no significant effect on thrombin-induced accumulation at any of the doses te sted. 5 Potentiation of in vivo platelet accumulation by dopamine therefore seems to occur via alpha-adrenergic receptors. However, the inhibitory effect of dopamine appears to be exerted via the activation of dopamine D1 receptors and not via beta-adrenergic receptors. Our Endings confirm that dopamine, but not adrenaline, can modify platelet function in the cerebral vasculatur e and these observations may have implications for current and potential th erapeutic uses of dopamine and selective dopaminergic compounds.