Potentiation and inhibition by clonidine of PAF-acether-induced human platelet activation

Abstract

PAF-acether (platelet-activating factor) and adrenaline synergized to induce aggregation of human platelets in whole blood and in platelet-rich plasma (PRP) irrespective of the use of citrate, of heparin or acid-citrate dextrose (ACD) as anticoagulants, whereas the partial adrenoceptor agonist clonidine imitated adrenaline in a limited number of cases and only when blood was collected in ACD. Whether added to ACD-PRP or ingested by the blood donors, aspirin suppressed the synergic effect of clonidine plus PAF-acether in plasma but failed to block the potentiated aggregation of adrenaline plus PAF-acether. Clonidine alone had no effect on plasma-free platelet suspensions and also failed to synergize with PAF-acether under conditions where the latter's association to adrenaline consistently induced full aggregation. Added before adrenaline or before adrenaline plus PAF-acether, clonidine reduced the aggregation to the level of that due to PAF-acether alone irrespective of cyclooxygenase inhibition with aspirin. The α 2-adrenoceptor antagonist yohimbine blocked the synergistic effects of adrenaline or clonidine associated to PAF-acether, reducing aggregation to that due to PAF-acether alone. Clonidine has dual effects on human platelets, since it can imitate adrenaline and synergize with PAF-acether in some subjects, and can also block aggregation induced by adrenaline alone or in combination with PAF-acether.