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.
- calcium-activated potassium channel
- patch clamp
- potassium transport