Involvement of K+ channels in the augmented nasal venous responsiveness to nitric oxide in rat model of allergic rhinitis

ObjectiveOne of the factors of nasal obstruction observed in allergic rhinitis is thought to be a dilatation of microveins in nasal mucosa, although the exact mechanism(s) is not fully understood. In nasal mucosae of repeatedly antigen challenged rats, NO-induced venodilatation itself is augmented. In the present study, the roles of K+ channels in sodium nitroprusside (NO donor; SNP)-induced venodilatation of nasal mucosae in antigen-challenged rats were investigated.MethodsActively sensitized rats were repeatedly challenged with aerosolized antigen. Twenty-four hours after the final antigen challenge, nasal septum mucosa was exposed surgically and observed directly in vivo under a stereoscopic microscope. The 20 μl reagents were administered onto the exposed septal mucosal surface, and the venous diameters of nasal mucosa were observed.ResultsThe SNP-induced venodilatation of septal mucosa was markedly and significantly increased in the antigen-challenged rats. The SNP-induced venodilatation was significantly inhibited by pretreatment with either tetraethylammonium [TEA; a large-conductance Ca2+ activated-K+ (KCa) and voltage dependent K+ (Kv) channel inhibitor] or glibenclamide [an ATP sensitive K+ (KATP) channel inhibitor].ConclusionsThese findings suggest that NO-induced venodilatation is augmented in nasal mucosae of challenged rats, and K+ channels play an important role in the augmented venous responsiveness to NO in nasal mucosae of repeatedly antigen challenged rats.

Graphical AbstractFigure optionsDownload as PowerPoint slideResearch Highlights
► Nasal venous responsiveness to NO is augmented in rat with allergic rhinitis.
► The NO-induced venodilatation is mediated by TEA-sensitive K+ channels.
► Also, the NO-induced venodilatation is inhibited by glibenclamide.
► Augmented K+ channels activities might be involved in rhinostenosis.