Lipid mediators such as prostaglandins and leukotrienes exacerbated nasal congestion in allergic rhinitis (AR) by increasing blood flow and vascular permeability in nasal mucosa. We here aimed to investigate the effect of a lipoxygenase-metabolite of dihomogammalinolenic acid, 15-hydroxyeicosatrienoic acid (15-HETrE) on functional changes of vasculature, since the previous study showed high level of 15-HETrE was detected in the nasal lavage fluid of AR mouse models. Intranasal administration of 15-HETrE caused abdominal breathing, decreased nasal cavity volume, and increased extravasation of dye injected intravenously in mice. Whole-mount immunostaining revealed that 15-HETrE administration relaxed vessels in nasal mucosa. In ex vivo experiments, the treatment of 15-HETrE relaxed mouse aorta pre-contracted by U46619 in a dose-dependent manner. This 15-HETrE-induced relaxation was inhibited by pre-treatment of prostaglandin D₂ receptor (DP) or prostacyclin receptor (IP) antagonists. Accordingly, the treatment of 15-HETrE on aorta tended to increase the level of intracellular cAMP. Finally, we showed 15-HETrE was detected in patients who complains of AR-related symptoms. These results indicate 15-HETrE can be a novel exacerbating lipid mediator for nasal congestion which stimulates major prostaglandin receptors DP and IP.