Nicotine increases basal prostacyclin production and DNA synthesis of human endothelial cells in primary cultures.

In order to better understand the direct effects of nicotine on the metabolism of human vascular endothelial cells we studied the effect of the drug on prostacyclin (PGI2) production and cellular proliferation. This study was performed in an in vitro model of primary cultures of human umbilical vein endothelial cells. PGI2 level was measured with a radioimmunoassay of 6-keto-PGF1 alpha secreted into culture medium. We observed that incubating the cells with nicotine resulted in a dose-dependent increase of the basal level of PGI2; however, at high doses, nicotine, tended to decrease the capacity of production obtained by thrombin stimulation. Endothelial cell growth was stimulated by nicotine with a maximal effect at 0.05 microgram/ml nicotine. We conclude that nicotine appeared, in some experimental conditions, to stimulate some parameters of endothelial cell metabolism and particularly prostacyclin production. Our results stress the importance of the experimental conditions, and may provide an explanation for the disparities of results in the literature. The results are discussed in relation to smoking induced vascular alteration.