Taste Receptors Type 2 Would Not Mediate Bitter Tastant-Induced Relaxation of Airway Smooth Muscle

Submit Manuscript | http://medcraveonline.com pre contraction through large-conductance Ca2+-activated K+ channels (BKs)[2,3]. However, our and others’ results indicate that the relaxation would not be mediated by BKs, which will result from the inhibition of L-type voltage-dependent Ca2+ channels (LVDCCs) and non-selective cat ion channels (NSCCs) [47]. These studies clarified the paradox about the mechanism of bitter Tastant-induced relaxation. Bitter tastants induce Ca2+ store release leading to cytosolic Ca2+ increases through the TAS2R-Gβγ protein-PLCβ-IP3-IP3R pathway, however, the increased Ca2+ does not cause a contraction [5,8]. This would be because that the increase of Ca2+ did not reach the threshold level of triggering a contraction, which might be due to that bitter tastants inhibited Ca2+ release channels such as ryanodine receptors (RyRs) and IP3 receptors (IP3Rs), since that bitter tastants blocked caffeine (an activator of RyRs)-induced cytosolic Ca2+ increases [7] and ACHinduced Ca2+ oscillations mediated by IP3R-induced Ca2+ release [9,10]. Thereby, bitter Tastant-induced Ca2+ release would be inhibited, leading to that the cytosolic Ca2+ cannot increase to the level for evoking a contraction.