1 The¯avonol quercetin has been shown to activate a Cl 7 secretion in rat colon. Unlike the secretory activity of the related iso¯avone genistein, quercetin's secretory activity does not depend on cyclic AMP; instead, it depends on Ca 2+ . We investigated the possible involvement of Ca 2+ dependent basolateral K + channels using apically permeabilized rat distal colon epithelium mounted in Ussing chambers. 2 In intact epithelium, quercetin induced an increase in short-circuit current (I sc ), which was diminished by the Cl 7 channel blockers NPPB and DPC, but not by glibenclamide, DIDS or anthracene-9-carboxylic acid. The e ect of the¯avonol was also inhibited by several serosally applied K + channel blockers (Ba 2+ , quinine, clotrimazole, tetrapentylammonium, 293B), whereas other K + channel blockers failed to in¯uence the quercetin-induced increase in I sc (tetraethylammonium, charybdotoxin). 3 The apical membrane was permeabilized by mucosal addition of nystatin and a serosally directed K + gradient was applied. The successful permeabilization was con®rmed by experiments demonstrating the failure of bumetanide to inhibit the carbachol-induced current. 4 In apically permeabilized epithelium, quercetin induced a K + current (I K ), which was neither in¯uenced by ouabain nor by bumetanide. Whereas DPC, NPPB, charybdotoxin and 293B failed to inhibit this I K , quinine, Ba 2+ , clotrimazole and tetrapentylammonium were e ective blockers of this current. 5 We conclude from these results that at least part of the quercetin-induced Cl 7 secretion can be explained by an activation of basolateral K + channels.