Multiple effects of arginine vasopressin on prostaglandin E₂ synthesis in fibroblasts

Recent evidence supports the viewpoint that vasopressin, a neurohypophyseal peptide, should be also considered as a neuroendocrine modulator of immune and inflammatory responses. In this work we investigated the role of vasopressin in the regulation of prostaglandin E₂ synthesis by human dermal fibroblasts. Recombinant human interleukin-1β increased prostaglandin E₂ synthesis in fibroblasts about sixfold. The prostaglandin E₂ response to interleukin-1β was attenuated by lower concentrations of vasopressin (10^-10-10^-9 M). By contrast, higher concentrations (10^-8-10^-7 M) of vasopressin effected significant enhancement of the interleukin-1β-induced prostaglandin E₂ synthesis. In a similar way, vasopressin (10 ^-8-10^-7 M), in the absence of interleukin-1, significantly increased prostaglandin E₂ production. An inhibitory effect of lower concentrations of vasopressin was also observed on basal production of prostaglandin E₂. The effects of vasopressin on basal and interleukin-1β-induced prostaglandin E₂ synthesis were antagonized by selective vasopressin receptor antagonists. The findings presented here disclose a novel modulatory role of vasopressin on prostaglandin E₂ synthesis in human dermal fibroblasts and suggest a possible role of vasopressin in the regulation of inflammation.