Vascular substances that modulate blood-to-vessel interactions.
The vessel wall contains powerful inhibitors of thrombogenesis. One substance, a proteoglycan, is a strong anticoagulant but has only a limited effect on platelet aggregation. It prolongs the thrombin clotting time and partial thromboplastin time, but only blocks platelet aggregation induced by thrombin. Another vessel wall constituent, a prostaglandin derivative (prostacyclin), is a potent inhibitor of platelet aggregation. It antagonizes platelet aggregation induced by a variety of agents including adenosine diphosphate, collagen, arachidonic acid and thrombin; however, its only effect on coagulation is through the inhibition of platelet factor-3 release. Proteoglycans and prostacyclin comlement each other's antithrombotic activities, and together serve to limit the hemostatic response of blood to vessel wall injury. Vessels devoid of the intima continue to produce prostacyclin. Prostacyclin produced by these vessels is probably more important than that produced by vessels with the intima in the prevention of thrombus deposition.
D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology; D001158:Arteries / Q000502:physiology*; D001777:Blood Coagulation; D002417:Cattle; D011464:Epoprostenol / Q000502:physiology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000502:physiology*; D011509:Proteoglycans / Q000502:physiology*; D051381:Rats
D011453:Prostaglandins; D011509:Proteoglycans; D011464:Epoprostenol