AJP - Gastrointestinal and Liver Physiology, Vol 250, Issue 1 35-G43, Copyright © 1986 by American Physiological Society
Na-H exchange in rat liver basolateral but not canalicular plasma membrane vesicles
R. H. Moseley, P. J. Meier, P. S. Aronson and J. L. Boyer
Na+-stimulated H+ movement and H+-stimulated Na+ uptake were studied in
basolateral (blLPM) and canalicular (cLPM) rat liver membrane vesicles. H+
movement was monitored with the fluorescent amine acridine orange; 22Na
uptake was assayed by a rapid Millipore filtration technique. In blLPM,
inwardly directed Na+ gradients stimulated H+ efflux and outwardly directed
Na+ gradients stimulated proton influx. Outwardly directed proton gradients
(pH in 5.9/pH out 7.9) stimulated initial 22Na uptake rates 5- to 10-fold
over pH-equilibrated conditions (pH in 7.9/pH out 7.9). Conversely,
inwardly directed proton gradients (pH in 7.9/pH out 5.9) inhibited 22Na
uptake. pH-dependent 22Na uptake was inhibited by amiloride and harmaline
but not by other transport inhibitors, bumetanide, furosemide,
4,4'-diisothiocyano-2,2'-disulfonic acid stilbene,
4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, and
acetazolamide. Lithium also inhibited H+-stimulated 22Na uptake. Although a
component of pH-stimulated 22Na uptake appeared to be dependent on membrane
potential, this electrogenic component was amiloride insensitive. Proton
gradient-stimulated 22Na uptake in blLPM was saturable, with a Km of 5.4 mM
and a Vmax of 14 nmol . min-1 . mg prot-1. In contrast, in cLPM, no Na+
gradient-stimulated proton movement and no pH-dependent Na+ uptake
occurred. These findings establish an electroneutral Na-H antiport in blLPM
but not cLPM in rat liver. The polarity of this exchanger supports a model
of bile formation that is dependent, in part, on canalicular HCO-3 and/or
OH- excretion.
