Endothelin (ET)‐1 is a 21‐amino acid peptide which has vasoconstrictor and growth regulatory activity. Recently, cultured keratinocytes have been reported to express ET‐1 and its receptor when irradiated by ultraviolet (UV) B. In order to further understand the role of ET‐1 in vivo during UVB‐induced inflammation, we examined the localization, intensity and time course of the expression levels of ET‐1 and its binding sites in UVB‐exposed BALB/c mouse skin. Frozen and paraffin sections prepared from mouse skin 48 h after treatment with UVB irradiation (0.36 or 0.72 J/cm²) or after injection with tumor necrosis factor (TNF)‐α (1.0 μg) or interleukin (IL)‐1α (0.05 μg) were incubated with monoclonal anti‐ET‐1 IgG and then visualized by peroxidase staining. In normal skin, faint ET‐1 immunoreactivity was observed in the epidermis, pilosebaceous structures and blood vessels. Upon exposure to UVB irradiation or administration of TNF‐α injection or IL‐1α injection, such immunoreactivity was found to be significantly enhanced. Subsequently, the frozen sections were incubated with ¹²⁵I ET‐1 for 30 min, and visualized by autoradiographic technique. In normal skin, ET‐1 weakly bound to the skin, while UVB irradiation and TNF‐α injection significantly enhanced ET‐1 binding in the epidermis, pilosebaceous structures and blood vessels. Time course experiments (1, 2, 4 and 7 days) indicated that ET‐1 immunoreactivity and ET‐1 binding peaked 1 or 2 days after UVB irradiation or TNF‐α injection. These results suggest that the up‐regulated expression of ET‐1 and its binding sites in the epidermis and pilosebaceous structures may act as an autocrine/paracrine factor during UVB‐induced inflammation.