The study demonstrates that ristocetin-induced platelet aggregation is a passive process involving membrane binding rather than active platelet metabolism.
Questions active platelet metabolism in ristocetin aggregation; leaves open relevance to human vWF diagnostics.
Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin-induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.
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Kattlove et al. (1975) studied this question.
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