Upon allergic rhinitis (AR), various inflammatory mediators increase blood flow and vascular permeability in nasal mucosa, which result in nasal congestion.
We here investigated the effects of 15-hydroxyeicosatrienoic acid (15-HETrE) on functional changes of vasculature and nasal congestion in mice.  In isolated mouse aorta, the treatment of 0.1-3 µM 15-HETrE itself did not induce any contraction but inhibited the TP agonist (U46619)-induced contraction in a dose-dependent manner. Several lipid mediators are known to cause vasodilation by activating K⁺ channels. Consistently, a pre-treatment of BKCa/IKCa, K_V, or K_ATP channel inhibitor inhibited the 15-HETrE-induced relaxation. In vivo, the topical administration of 1 µg U46619 constricted vein in mouse ear. A pre-administration of 1 µg 15-HETrE also inhibited the U46619-induced vein constriction. In modified Mile’s assay, an intranasal administration of 20 µg 15-HETrE increased dye extravasation in the nasal mucosa. This administration also induced abdominal breathing, immobility, and lying down, which can be caused by nasal congestion. Thus, 15-HETrE induced vasorelaxation and vascular hyperpermeability. These phenomena presumably contribute to nasal congestion.