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Department of Physiology and Biophysics, Cornell University Medical College, New York, New York 10021
A mathematical model of the inner medullary collecting duct
(IMCD) of the rat has been developed that is suitable for simulating luminal buffer titration and ammonia secretion by this nephron segment.
Luminal proton secretion has been assigned to an H-K-ATPase, which has
been represented by adapting the kinetic model of the gastric enzyme by
Brzezinski et al. (P. Brzezinski, B. G. Malmstrom, P. Lorentzon, and B. Wallmark. Biochim. Biophys. Acta 942: 215-219, 1988). In
shifting to a 2 H+:1 ATP stoichiometry, the model enzyme
can acidify the tubule lumen ~3 pH units below that of the cytosol,
when luminal K+ is in abundance. Peritubular base exit is a
combination of ammonia recycling and
HCO
3 flux (either via
Cl/HCO3 exchange or via a
Cl channel). Ammonia recycling involves
NH+4 uptake on the Na-K-ATPase
followed by diffusive NH3 exit [S. M. Wall. Am. J. Physiol. 270 (Renal Physiol. 39): F432-F439, 1996];
model calculations suggest that this is the principal mode of base
exit. By virtue of this mechanism, the model also suggests that
realistic elevations in peritubular K+ concentration will
compromise IMCD acid secretion. Although ammonia recycling is
insensitive to carbonic anhydrase (CA) inhibition, the base exit linked
to HCO3 flux provides a CA-sensitive
component to acid secretion. In model simulations, it is observed that
increased luminal NaCl entry increases ammonia cycling but decreases
peritubular Cl/HCO3 exchange (due to increased cell Cl). This parallel
system of peritubular base exit stabilizes acid secretion in the face
of variable Na+ reabsorption.
epithelial proton transport; proton-potassium-adenosinetriphosphatase; chloride/bicarbonate exchange; ammonia transport
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