Alpha2-adrenoceptor antagonists and imidazoline agents effectively inhibit adrenaline-potentiated platelet aggregation in canine models.
Should not alter clinical antiplatelet practice; leaves open translation of canine anti-aggregation effects to humans.
Aggregatory and antiaggregatory effects of imidazol(in)e and non-imidazol(in)e alpha-adrenergic agents on canine platelets were examined turbidimetrically in citrated platelet-rich plasma or washed platelet solution. Each alpha-adrenoceptor agonist alone did not induce aggregation, but adrenaline and noradrenaline potentiated dose-dependently aggregation stimulated by ADP, collagen or thrombin. Small potentiation of ADP- or collagen-stimulated aggregation was also observed in response to oxymetazoline. The alpha2-adrenoceptor antagonists and/or imidazol(in)e alpha-adrenergic agents inhibit dose-dependently adrenaline-potentiated aggregation, whereas alpha1-adrenoceptor antagonists, a beta-adrenoceptor antagonist and non-imidazol(in)e alpha-adrenergic agents were no or less effective in inhibiting adrenaline-potentiated aggregation. The alpha2-adrenoceptor agonists did not reduce inhibitory effect of alpha2-adrenoceptor antagonists for adrenaline-potentiated aggregation. The alpha2-adrenoceptor antagonists and/or imidazol(in)es were no or less effective in inhibiting aggregation induced by ADP or thrombin alone. These results demonstrated that alpha2-adrenoceptor-blocking agents and/or imidazol(in)e alpha-adrenergic agents inhibit effectively the adrenaline-potentiated platelet aggregation.
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Hikasa et al. (1999) studied this question.
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