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Endothelial cells were isolated from human umbilical cord and cultured by the modified method of Jaffe et al. The supernatant over the monolayer of endothelial cells cultured for 5-7 days and growing confluent, was tested as the material of this experiment. The supernatant demonstrated an inhibitory effect for ADP induced platelet aggregation, and this effect was increased by addition of arachidonic acid (10μM), and was diminished by the pretreatment with acetylsalicylic acid (100μM) for 1hr. By means of thin layer radio-chromatography of the supernatant, it was identified that this antiaggregating effect was developed by prostacyclin released from endothelial cells. Suspended endothelial cells were incubated with several drugs in order to evaluate the prostacyclin generation from endothelial cells, and assayed by RIA as 6-keto PGF1α. Prostacyclin synthesis increased in 25 folds by addition of arachidonic acid. Nitroglycerin increased prostacyclin synthesis of endothelial cells, but hydralazine and verapamil did not increase it. Through these experimental results, it was concluded that effect of these vasodilators was possibly developed by the increase of prostacyclin synthesis from endothelial cells.
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