The influence of nicotine on the production of prostacyclin was studied in umbilical arteries from newborn infants of mothers who were smokers and those who were non-smokers. Thirteen umbilical cords were obtained from the non-smokers and 10 from the smokers. After their ability to produce prostacyclin was shown, the arteries were perfused during a 20 minute period with nicotine 10-7 mol in Krebs-Henseleit buffer and then again during 20 minutes with pure buffer. Nicotine led to a decline in prostacyclin production in all but one artery. In five of 12 arteries from mothers who did not smoke the production recovered during buffer reperfusion, while in nine of 10 arteries from mothers who smoked, prostacyclin production declined to lower levels and did not increase during 20 minutes buffer reperfusion. It is concluded that nicotine has a direct depressive effect on the prostacyclin production in the vascular wall, which in turn may lead to increased platelet aggregation and thus be a precursor of vascular lesions.