BACKGROUND: Endothelin(ET) is a very potent vasoconstrictive peptide produced by endothelial cells of pulmonary artery. The endothelin level was increased in plasma of primary pulmonary hypertension and acute pulmonary thromboembolism and it was suggested that the endothelin might do a critical role in the cardiopulmonary dysfunction in these two conditions. But the exact mechanism of increase of ET has not been known. In these two conditions, platelet activation and thrombosis are the main pathophysiologic findings. So there is a possibility that the platelet might stimulate endothelin secretion from endothelial cells. Therefore, we performed this study to evaluate the role of platelet and its mediators on endothelin production in bovine pulmonary artery endothelial(BPAE) cells. METHOD: Bovine pulmonary artery endothelial cells, ATCC certified cell line 209, were cultured and treated with human platelets(106-108/ml), thrombin (0.1~10u/ml), TGF-beta1(1~1000pM), serotonin(1~100uM), and endotoxin(1ug/ml) in a final volume of 500ul for 18 hours. Levels of ir(immunoreactive)-ET in each conditiond medium were measured by a radioimmunoassay specific for ET. RESULT: The increase of ir-FT levels was platelet number and time dependent over 18 hours. When washed human platelets were added(108/ml), the ir-ET levels were significantly higher than that of control(p<0.05) at 8 and 18 hours after culture. Subtbreshold concentration of platelets(107ml) coincubated with endotoxin( lug/ml) or subtbreshold dose of thrombin(0.1u/ml) stimulated ir-ET secretion from BPAE cells significantiy(p<0.05) compared with control. Thrombin(1ug/ml, 10ug/ml) and TGF-beta1(100pM, 1000pM) significantly increased ir-ET secretion from BPAE cells(p<0.05) compared with control, but serotoin(1-100uM) and endotoxin(1ug/ml) did not stimulate the ir-ET secretion. CONCLUSIONS: Platelets stimulate endotheiin secretion from bovine pulmonary artery endothelial cells. The mechanism of increase of endotheiin secretion seems to be a stimulation by platelet itself or by mediators, such as TGF-beta1, secreted from activated platelets. And, in this study, the priming effect of platelets on endothelin secretion from BPAE cells could be another possibility.