Abstract
PROSTACYCLIN (PGI2) was reported by Vane and co-workers as a novel short-lived metabolite of prostaglandin endoperoxides (PGG2 and PGH2) which inhibited platelet aggregation1. Subsequent studies have demonstrated that PGI2 is the most potent inhibitor of platelet aggregation so far described, acting by stimulating platelet adenylate cyclase2–4. PGI2 is produced by isolated blood vessel segments5 and is therefore likely to be of great importance in the maintenance of vascular homeostasis. The cellular localisation and regulation of PGI2 synthesis have not previously been established, although it has been proposed that the main source of PGI2 is through pro-aggregatory prostaglandin endoperoxides released from platelets being enzymatically converted to PGI2 by vascular endothelial cells5,6. We show here that pig aortic endothelial cells, but not aortic smooth muscle cells or fibroblasts, synthesise PGI2. This production of PGI2 is stimulated by incubating endothelial cells with PGG2 or with its precursor, arachidonic acid. Furthermore, PGI2 synthesis is powerfully stimulated by cell-free plasma.
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MACINTYRE, D., PEARSON, J. & GORDON, J. Localisation and stimulation of prostacyclin production in vascular cells. Nature 271, 549–551 (1978). https://doi.org/10.1038/271549a0
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DOI: https://doi.org/10.1038/271549a0
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