Referenced in: none

Automatically associated channels: Kv10.1

Title: Involvement of K(+) channels in the augmented nasal venous responsiveness to nitric oxide in rat model of allergic rhinitis.

Authors: Hiroyasu Sakai, Jun Enzaka, Michiko Sakai-Oshita, Futa Uto, Yoshihiko Chiba, Miwa Misawa

Journal, date & volume: Microvasc. Res., 2011 Jan , 81, 129-34

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21108952

Abstract
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.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 20μl reagents were administered onto the exposed septal mucosal surface, and the venous diameters of nasal mucosa were observed.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].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.