Human serum, plasma, and platelets stimulate prostacyclin and endothelin-1 synthesis in human vascular endothelial cells.

Prostacyclin (PGI2), a powerful vasodilatory prostanoid, and endothelin-1 (ET-1), a potent vasoconstrictive peptide, are produced by vascular endothelial cells. We show that human serum (10%) caused a 3.2-fold stimulation both in PGI2 and ET-1 synthesis in human endothelial cells cultured from umbilical veins, and human plasma (10%) stimulated productions of both 1.6- and 1.7-fold, respectively. In addition, releasates from thrombin-activated platelets (20 x 10(9) platelets/l) caused a 1.9-fold increase in PGI2 and a 1.4-fold increase in the ET-1 synthesis. Releasates from frozen-thawed and sonicated platelets (20 x 10(9) platelets/l) caused a 3.6-fold increase in PGI2 release but did not affect ET-1 production. We thus conclude that, in normal situation, endothelial stimulating activity present in plasma perhaps plays a role in the regulation of endothelial function, whereas platelet-derived activity in serum may be important at site of thrombosis.