Stimulation of prostacyclin biosynthetic activity by estradiol in rat aortic smooth muscle cells in culture.
Effects of estradio on cell proliferation and prostacyclin biosynthetic activity in cultured rat aortic smooth muscle cells are investigated. Prostacyclin is the major product formed from arachidonic acid by the cells, both in a cell-free homogenate system and in intact cells. When cells are treated with estradiol, no effect on cell proliferation is observed. However, a significantly stimulatory effect on prostacyclin biosynthetic activity in cells is evident. The maximal effect of estradiol on the stimulation of prostacyclin biosynthetic activity is observed after 5-day treatment of the cells with estradiol at its physiological concentration (10(-9) M). Our results support the idea that estradiol would be a protective hormone in atherosclerotic heart disease.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism; D001095:Arachidonic Acids / Q000378:metabolism / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000096:biosynthesis*; D004958:Estradiol / Q000494:pharmacology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D013997:Time Factors
D001095:Arachidonic Acids; D011453:Prostaglandins; D004958:Estradiol; D000244:Adenosine Diphosphate; D011464:Epoprostenol