Physico-chemical Interaction between Adenosine Phosphates and Fibrinogen as a Cause of Platelet Aggregation

Abstract

PLATELETS in a citrated or heparinized plasma system, adhere to each other to form aggregates in the presence of low concentrations of adenosine diphosphate (ADP)¹. Adenosine monophosphate (AMP) and adenosine are ineffective in this respect and indeed act as inhibitors of aggregation by ADP². The degree of aggregation depends on the rate of stirring and, consequently, on the collision frequency of the cells, which is an indication that the process causing aggregation occurs at or very close to the platelet surface. Born and Cross³ and Cross⁴ showed that fibrinogen acts as a co-factor for aggregation, and Deykin et al.⁵ suggested that another plasma protein may also be required. Although Born⁶ and Hampton and Mitchell⁷ found that ADP is taken up immediately by specific receptors at the surface of the platelets, the mechanism of this type of aggregation is still obscure. Born concluded that “platelet aggregation by ADP comes about through a reaction in which each ADP molecule is briefly involved to produce an alteration in another component of the system, for example in the receptor or in the protein co-factor, without necessarily being altered itself”.