Prostacyclin release from cultured and ex vivo bovine vascular endothelium. Studies with thrombin, arachidonic acid, and ionophore A23187.
Prostacyclin release from systemic and pulmonary endothelium has been evaluated in cultured cell monolayers and in an ex vivo vascular segment model in which the endothelium remains in contact with subendothelial structures. The effect of exposure to arachidonic acid, ionophore A23187, and thrombin on prostacyclin release has been assessed. Arachidonic acid elicited prostacyclin release in a dose-dependent fashion. Ionophore also stimulated bovine systemic endothelium to release prostacyclin. Thrombin-endothelial cell interactions have been examined extensively. Unlike umbilical venous endothelium, systemic and pulmonary bovine endothelium did not release prostacyclin following exposure to thrombin. Exposure to thrombin also failed to evoke the release of tritiated arachidonate metabolites from the bovine endothelial cell preparations. The presence of high affinity binding sites for thrombin (KD = 9.5 X 10(-9) M) on the bovine endothelium suggests that either thrombin binding is causally unrelated to prostacyclin release or that the bovine cells lack mediators required for thrombin to exert its effect.