The role of the kidney in combating
metabolic acidosis has been a subject of considerable interest for many years. The present study was aimed to determine whether there is an altered regulation of renal
acid base transporters in acute and chronic
acid loading. Male Sprague-Dawley rats were used.
Metabolic acidosis was induced by administration of NH(4)Cl for 2 days (acute) and for 7days (chronic). The serum and urinary pH and
bicarbonate were measured. The
protein expression of renal
acid base transporters [type 3
Na(+)/H(+) exchanger (NHE3), type 1 Na(+)/HCO(3) (-) cotransporter (NBC1), Na-K(+)
ATPase, H(+)-
ATPase,
anion exchanger-1 (AE-1)] was measured by semiquantitative immunoblotting. Serum
bicarbonate and pH were decreased in acute
acid loading rats compared with controls. Accordingly, urinary pH decreased. The
protein expression of NHE3,
H(+)-ATPase, AE-1 and NBC1 was not changed. In chronic
acid loading rats, serum
bicarbonate and pH were not changed, while urinary pH was decreased compared with controls. The
protein expression of NHE3,
H(+)-ATPase was increased in the renal cortex of chronic
acid loading rats. These results suggest that unaltered expression of
acid transporters combined with acute
acid loading may contribute to the development of
acidosis. The subsequent increased expression of NHE3,
H(+)-ATPase in the kidney may play a role in promoting
acid excretion in the later stage of
acid loading, which counteract the development of
metabolic acidosis.