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Departments of Cellular and Molecular Physiology and of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8026
In metabolic
acidosis, the capacity of the proximal tubule for
bicarbonate absorption is enhanced, whereas NaCl reabsorption is
inhibited. Recent evidence indicates that transcellular NaCl absorption
in the proximal tubule is mediated by apical membrane Cl
/formate exchange and
Cl/oxalate exchange, in
parallel with recycling of these organic anions. We evaluated whether
the effect of metabolic acidosis to inhibit NaCl reabsorption in the
proximal tubule is due at least in part to inhibition of organic
anion-dependent NaCl transport in this nephron segment. Absorption
rates of bicarbonate
(JHCO3), chloride (JCl),
and fluid (Jv)
were measured in rat proximal tubule segments microperfused in situ. We
confirmed that metabolic acidosis stimulates
JHCO3
in tubules microperfused with 25 mM HCO3, pH 7.4. For measurements of
JCl, tubules were
microperfused with a low-bicarbonate (5 mM), high-chloride solution,
simulating conditions in the late proximal tubule. Under these
conditions, baseline
JCl and
Jv measured in
the absence of formate and oxalate were not significantly different
between control and acidotic rats. However, whereas addition of 50 µM formate or 1 µM oxalate to luminal and capillary perfusates markedly stimulated JCl
and Jv in control
rats, formate and oxalate failed to stimulate
JCl and
Jv in acidotic
rats. We conclude that metabolic acidosis markedly downregulates
organic anion-stimulated NaCl absorption, thereby allowing differential
regulation of proximal tubule
NaHCO3 and NaCl transport.
pH; anion exchange; formate; oxalate; sodium/proton exchange
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