Abstract
Objective One 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. Methods Actively 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. Results The 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 Ca 2+ activated-K + (K Ca) and voltage dependent K + (Kv) channel inhibitor] or glibenclamide [an ATP sensitive K + (K ATP) channel inhibitor]. Conclusions These 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.
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