Cigarette smoke extracts, but not nicotine, inhibit prostacyclin (PGI2) synthesis in human, rabbit and rat vascular tissue.
Ethanolic and aqueous cigarette smoke extracts were tested for their influence on prostacyclin (PGI2) synthesis in four vascular models: human umbilical artery, rabbit aorta, rat aorta and rat lung. Nicotine was also studied. In each tissue, a dose-dependent inhibition of the release of PGI2 (assessed by measurement of immunoreactive 6-oxo-PGF1 alpha, the stable hydrolysis product of PGI2), was seen on incubation with aqueous or ethanolic cigarette smoke extracts; nicotine, at concentrations of up to 1 g/1, was without effect. In vitro conversion of [14C]-arachidonic acid to [14C]-6-oxo-PGF1 alpha by human umbilical artery was also inhibited by both ethanolic and aqueous cigarette smoke extracts, whereas nicotine was again without effect. We conclude that cigarette smoke inhibits PGI2 synthesis at the level of cyclooxygenase or beyond it, and that components other than nicotine are responsible for this effect. In blood vessels, the inhibition of PGI2 synthesis may contribute to the pathogenesis of the vascular complications of smoking.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D001158:Arteries / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D066298:In Vitro Techniques; D008168:Lung / Q000378:metabolism; D009538:Nicotine / Q000633:toxicity*; D010947:Plants, Toxic; D011817:Rabbits; D011863:Radioimmunoassay; D051381:Rats; D012906:Smoke; D014026:Nicotiana
D012906:Smoke; D015121:6-Ketoprostaglandin F1 alpha; D009538:Nicotine; D011464:Epoprostenol