Abstract
Platelets aggregate with thrombin-free autoprothrombin II-A. Aggregation was dependent on an intact release mechanism since inhibition of aggregation occurred with adenosine, colchicine, or EDTA. Autoprothrombin II-A reduced the sensitivity of platelets to aggregate with thrombin, but enhanced epinephrine-mediated aggregation. Autoprothrombin II-A directly competes for membrane sites sensitive to thrombin. It allows complexes to from with epinephrine. There was no absolute requirement for autoprothrombin II-A since epinephrine aggregated dog platelets at the identical optimum concentration following Coumadin treatment.
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