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Deshpande et al. 1 reported that bitter tastants increase intracellular Ca2+ concentration (to similar levels produced by the bronchoconstrictive agonists histamine and bradykinin) yet cause marked bronchodilation. This implies that elevated Ca2+ concentration inhibits contraction, challenging the classic Ca2+-dependent mechanism underlying smooth muscle contraction2, 3. To resolve this apparent paradox, the authors showed that bitter tastants can generate localized Ca2+ events, and that bitter tastantinduced relaxation and hyperpolarization can be inhibited by the largeconductance Ca2+-activated K+(BK) channel antagonist iberiotoxin1; thus, they propose that bitter tastant–induced bronchodilation results from its ability to generate localized Ca2+ signals, which in turn open BK channels and hyperpolarize the membrane. However, their assertion of the involvement of BK channel activation was solely based …