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• W2003673292 abstract "Although neurogenic inflammation via the activation of C-fibers in the airway may have an important role in the pathogenesis of asthma, their regulatory mechanism remains uncertain.The pharmacological profiles of a neuroactive steroid, allotetrahydrocorticosterone, on the activation of C-fibers in airway tissues were investigated, and the mechanism how a neuroactive steroid regulates airway inflammatory reactions was clarified.The effects of allotetrahydrocorticosterone on electrical field stimulation-induced bronchial smooth muscle contraction in guinea pig airway tissues were investigated. The influences of K+ channel blockers and intracellular protein inhibitors on the effects of allotetrahydrocorticosterone were examined.Allotetrahydrocorticosterone dose-dependently inhibited electrical field stimulation-induced guinea pig bronchial smooth muscle contraction. The inhibitory effects of allotetrahydrocorticosterone on electrical field stimulation-induced bronchial contraction were reduced by the pretreatment of Maxi-K+ channel blockers, iberiotoxin and charybdotoxin, but not other K+ channel blockers, dendrotoxin or glibenclamide. Pretreatment with pertussis toxin diminished the inhibitory effect of allotetrahydrocorticosterone, but not an adenylate cyclase inhibitor, SQ 22536, nor a specific inhibitor of mitogen-activated protein kinase kinase, PD 98059.These findings suggest that allotetrahydrocorticosterone negatively modulates the activation of C-fibers in guinea pig airway tissues via the opening of Maxi-K+ channels and a pertussis toxin-sensitive G-protein-coupled mechanism." @default.
• W2003673292 created "2016-06-24" @default.
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• W2003673292 date "2006-01-01" @default.
• W2003673292 modified "2023-10-13" @default.
• W2003673292 title "A Neuroactive Steroid Inhibits Guinea Pig Airway Sensory Nerves via Maxi-K⁺ Channel Activation" @default.
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• W2003673292 doi "https://doi.org/10.1159/000094179" @default.
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