Ba²⁺, TEA⁺, and quinine effects on apical membrane K⁺ conductance and maxi K⁺ channels in gallbladder epithelium

The apical membrane of Necturus gallbladder epithelium contains a voltage-activated K⁺ conductance [G(a)(V)]. Large-conductance (maxi) K⁺ channels underlie G(a)(V) and account for 17% of the membrane conductance (G(a)) under control conditions. We examined the Ba²⁺, tetraethylammonium (TEA⁺), and quinine sensitivities of G(a) and single maxi K⁺ channels. Mucosal Ba²⁺ addition decreased resting G(a) in a concentration-dependent manner (65% block at 5 mM) and decreased G(a)(V) in a concentration- and voltage-dependent manner. Mucosal TEA⁺ addition also decreased control G(a) (60% reduction at 5 mM). TEA⁺ block of G(a)(V) was more potent and less voltage dependent that Ba²⁺ block. Maxi K⁺ channels were blocked by external Ba²⁺ at millimolar levels and by external TEA⁺ at submillimolar levels. At 0.3 mM, quinine (mucosal addition) hyperpolarized the cell membranes by 6 mV and reduced the fractional apical membrane resistance by 50%, suggesting activation of an apical membrane K⁺ conductance. At 1 mM, quinine both activated and blocked K⁺-conductive pathways. Quinine blocked maxi K⁺ channel currents at submillimolar concentrations. We conclude that 1) Ba²⁺ and TEA⁺ block maxi K⁺ channels and other K⁺ channels underlying resting G(a); 2) parallels between the Ba²⁺ and TEA⁺ sensitivities of G(a)(V) and maxi K⁺ channels support a role for these channels in G(a)(V); and 3) quinine has multiple effects on K⁺ conductive pathways in gallbladder epithelium, which are only partially explained by block of apical membrane maxi K⁺ channels.