The Journal of General Physiology, Vol 89, 563-580, Copyright © 1987 by The Rockefeller University Press
Interaction between the basolateral K+ and apical Na+ conductances in Necturus urinary bladder
JR Demarest and AL Finn
Experimental modulation of the apical membrane Na+ conductance or
basolateral membrane Na+-K+ pump activity has been shown to result in
parallel changes in the basolateral K+ conductance in a number of
epithelia. To determine whether modulation of the basolateral K+
conductance would result in parallel changes in apical Na+ conductance and
basolateral pump activity, Necturus urinary bladders stripped of serosal
muscle and connective tissue were impaled through their basolateral
membranes with microelectrodes in experiments that allowed rapid serosal
solution changes. Exposure of the basolateral membrane to the K+ channel
blockers Ba2+ (0.5 mM/liter), Cs+ (10 mM/liter), or Rb+ (10 mM/liter)
increased the basolateral resistance (Rb) by greater than 75% in each case.
The increases in Rb were accompanied simultaneously by significant
increases in apical resistance (Ra) of greater than 20% and decreases in
transepithelial Na+ transport. The increases in Ra, measured as slope
resistances, cannot be attributed to nonlinearity of the I-V relationship
of the apical membrane, since the measured cell membrane potentials with
the K+ channel blockers present were not significantly different from those
resulting from increasing serosal K+, a maneuver that did not affect Ra.
Thus, blocking the K+ conductance causes a reduction in net Na+ transport
by reducing K+ exit from the cell and simultaneously reducing Na+ entry
into the cell. Close correlations between the calculated short-circuit
current and the apical and basolateral conductances were preserved after
the basolateral K+ conductance pathways had been blocked. Thus, the
interaction between the basolateral and apical conductances revealed by
blocking the basolateral K+ channels is part of a network of feedback
relationships that normally serves to maintain cellular homeostasis during
changes in the rate of transepithelial Na+ transport.
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