Autoprothrombin ii-a, thrombin, and epinephrine: interrelated effects on platelet aggregation.
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.
D000818:Animals; D001780:Blood Coagulation Tests; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology / Q000502:physiology*; D005164:Factor IX / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D010974:Platelet Aggregation; D013917:Thrombin / Q000494:pharmacology / Q000502:physiology*
D005164:Factor IX; D013917:Thrombin; D004837:Epinephrine