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Sodium butyrate (Sb) exhibits diverse biological properties that result in the inhibition of histone deacetylase, and this agent has been investigated as a therapeutic agent in several pathological conditions. Several studies have demonstrated that Sb inhibits hypercontraction of smooth muscle, including bronchial, placental, and tracheal smooth muscle, through modulation of ion channels and non-ion channels. In the present study, we investigated the effect of Sb on hypercontractility of airway smooth muscle and the underlying intracellular signaling cascade. Rat tracheal smooth muscle (TSM) strips were precontracted by acetylcholine, carbachol, and potassium-chloride, and subsequently incubated with Sb, and the relaxation was measured. Sb inhibited carbachol-, acetylcholine-, and KCl-induced hypercontractility, at concentrations that did not alter the resting tension of TSM strips. The inhibitory effect of Sb was abolished in the presence of verapamil, a non-selective Ca2+ channel blocker, and were partially attenuated in the absence of extracellular Ca2+ or in the presence of nifedipine, a selective Ca2+ channel blocker, and xestospongin, an inositol 1,4,5-trisphosphate [InsP3] receptor blocker. In addition, intracellular signaling including phosphorylation of phospholipase C and protein kinase C was also investigated. These findings indicate that Sb inhibits hypercontractility of airway smooth muscle by decreasing intr
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