The effect of nicotine on human endothelial cell release of prostaglandins and ultrastructure.

The acute and sub-acute effects of nicotine at concentrations between 10(-9)M and 10(-2)M on human umbilical vein endothelial cell release of prostacyclin and prostaglandin E2 and the sub-acute effect on the endothelial cell ultrastructure have been examined. The acute effect of nicotine on prostaglandin release has been assessed by measuring release of prostacyclin and prostaglandin E2 following stimulation of confluent monolayers of endothelial cells with A23187 in the presence of nicotine. The sub-acute effect has been assessed by measuring A23187 stimulated release of prostacyclin and prostaglandin E2 from endothelial cells grown to confluence in the presence of nicotine. The cell monolayers were also examined for morphological and ultrastructural changes using light and electron microscopy. Nicotine treated and untreated cells released minimal amounts of prostaglandin E2. Concentrations of nicotine between 10(-9)M and 10(-4)M did not inhibit release of prostacyclin or induce morphological changes. Acute exposure to 10(-3)M nicotine resulted in a statistically significant inhibition of prostacyclin release, however, sub-acute exposure did not inhibit prostaglandin release or effect the cell morphology. Acute and sub-acute exposure to 10(-2)M nicotine resulted in a statistically significant inhibition of prostacyclin release. This was accompanied by the appearance of large translucent cytoplasmic inclusions which did not appear to be lipid rich as indicated by the negative uptake of oil-red-O and osmium tetroxide. This study shows that concentrations of nicotine comparable to the plasma levels of smokers (10(-9)-10(-6)M) do not induce morphological changes or effect the release of endothelial prostaglandins.