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1 Medicine, University of Cincinnati, Cincinnati, OH, USA
2 Surgery, University of Cincinnati, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: hassane.amlal{at}uc.edu.
Metabolic acidosis is associated with alteration in fluid and electrolytes reabsorption in a number of nephron segments. However, the effect of metabolic acidosis on urine osmolality and collecting duct (CD) aquaporin-2 (AQP2) remain poorly understood. In these studies, we examined the effects of chronic metabolic acidosis on water handling by the kidney. Rats were placed in metabolic cages and subjected to control (water) or 280 mM NH<4Cl loading for five days to induce metabolic acidosis. The results indicated a significant increase in urine osmolality with no change in urine volume or urinary Na+ excretion in acid-loaded animals. This effect was independent of alteration in fluid intake or salt/chloride loading. Immunoblotting and Northern hybridization studies indicated that CD AQP2 protein abundance and mRNA expression levels increased significantly along the collecting duct system of NH4Cl- but not NaCl-loaded animals. Radioimmunoassay results indicated that acidosis was associated with a 4-fold increase in the circulating levels of vasopressin (AVP) and a 58% increase in brain AVP mRNA expression levels. In conclusion, metabolic acidosis upregulates the expression levels of collecting duct AQP2 and increases urine osmolality, suggesting an adaptive increase in water reabsorption in the CD. A concomitant increase in AVP synthesis and secretion likely plays an essential role in the adaptation of CD AQP2 in metabolic acidosis.
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