Cachectin/TNF as well as interleukin-1 induces prostacyclin synthesis in cultured vascular endothelial cells.
Cachectin/tumor necrosis factor (cachectin/TNF) has been shown to be capable of stimulating prostacyclin (PGI2) production by vascular endothelial cells in vitro. The stimulation of PGI2 by cachectin/TNF is comparable to that observed with interleukin-1, the monokine previously suggested to be the principal mediator of this effect. The ability of cachectin/TNF to stimulate PGI2 production suggests that it may play a role in producing depressed blood pressure or shock. If so, it might be possible to prevent such adverse effects with the aid of anti-inflammatory agents.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D006023:Glycoproteins / Q000494:pharmacology*; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha
D006023:Glycoproteins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol