AJP - Cell Physiology, Vol 259, Issue 1 C56-C68, Copyright © 1990 by American Physiological Society
Ba2+, TEA+, and quinine effects on apical membrane K+ conductance and maxi K+ channels in gallbladder epithelium
Y. Segal and L. Reuss
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.
The apical membrane of Necturus gallbladder epithelium contains a
voltage-activated K+ conductance [Ga(V)]. Large-conductance (maxi) K+
channels underlie Ga(V) and account for 17% of the membrane conductance
(Ga) under control conditions. We examined the Ba2+, tetraethylammonium
(TEA+), and quinine sensitivities of Ga and single maxi K+ channels.
Mucosal Ba2+ addition decreased resting Ga in a concentration-dependent
manner (65% block at 5 mM) and decreased Ga(V) in a concentration- and
voltage-dependent manner. Mucosal TEA+ addition also decreased control Ga
(60% reduction at 5 mM). TEA+ block of Ga(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 Ga; 2) parallels between the Ba2+ and TEA+ sensitivities
of Ga(V) and maxi K+ channels support a role for these channels in Ga(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.
