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Under normal physiologic conditions the receptor for F. VIII/VWF on human platelets is not readily available unless the antibiotic, ristocetin, is added. Searching for a physiologic mechanism inducing the receptor for F. VIII/VWF on human platelets, we found that low doses of thrombin (0.01-0.05 U/ml) induce steady state binding of 125I- F. VIII/VWF to human platelets. The binding is saturable and specific. Specificity was established by demonstrating that 100-fold molar excess of unlabeled F. VIII/VWF inhibited the binding while an excess of fibrinogen or fibro- nectin, two common contaminants of F. VIII/VWF, did not inhibit binding of 125I-F. VIII/VWF. Furthermore, rabbit antibody against F. VIII inhibited the binding. Thrombin- induced binding to human platelets can be observed only with fresh, metabolically active platelets. Glutaralde- hyde-treated platelets did not bind 125I-F. VIII/VWF following their treatment with thrombin, although they exhibited good binding in the presence of ristocetin. Thrombin appears to induce binding by acting on platelets rather than on F. VIII/VWF itself. Prostacyclin (PGI2 10-9M) inhibited thrombin-induced binding of 125I-F. VIII/VWF to human platelets, while ritcocetin-induced binding remained unaffected. Strikingly, PGI2-induced inhibition of binding was observed not orly when PGI2 was added before thrombin but also when PGI2 (10-9 M) was used 30 minutes after thrombin treatment and addition of 125I-F. VIII/VWF. Thus, binding of F. VIII/VWF to platelet receptor is induced by low concentrations of thrombin and is inhibited by PGI2. Since both agents are generated in the vicinity of injured vessel wall they may contribute to platelet-F. VIII/VWF- vessel wall interaction in vivo by regulating “up and down” platelet receptor for F. VIII/VWF.

The Receptor For Factor VIII/VWF On Human Platelets: Its Appearance And Disappearance Upon Action Of Thrombin And Prostacyclin