A previous study reported that intercellular adhesion molecule‐1 (ICAM‐1) expression by human vascular endothelial cells (HUVEC) is augmented by intracellular signal transmission mainly through the protein kinase C (PKC) system stimulated by TXA₂ receptors. In the present study, we show that a TXA₂ receptor agonist, U46619, augments the expression of not only ICAM‐1, but also vascular cell adhesion molecule‐1 (VCAM‐1) or endothelial leucocyte adhesion molecule‐1 (ELAM‐1) in HUVEC both at protein and mRNA levels. Pretreatment with SQ29,548 (a TXA₂ receptor antagonist) or PKC inhibitors greatly diminished the extent of U46619‐induced mRNA accumulation and surface expression of the adhesion molecules. An inhibitor of nuclear factor κB (NF‐κB) activation, PDTC, diminishes U46619‐induced VCAM‐1 mRNA accumulation. NAC, which inhibits NF‐κB and activation protein 1 (AP‐1) binding activity, inhibits the expression of ICAM‐1 or ELAM‐1 at protein and mRNA levels. These findings suggest that ICAM‐1 or ELAM‐1 expression of HUVEC stimulated via TXA₂ receptors is augmented by induction of NF‐κB and AP‐1 binding activity through the PKC system, and that VCAM‐1 expression is augmented by induction of NF‐κB binding activity.