Abstract

Although chronic metabolic acidosis results in an adaptive increase in the renal capacity to produce NH3, the response to a low pH produced by chronic respiratory acidosis is unknown. Rats were placed in a specially constructed chamber with an ambient CO2 of 10% for 3 days, which increased their PCO2 to 76 +/- 4 mmHg. NH3 production was determined in vitro using both isolated kidneys perfused with 0.5 mM glutamine and cortical tubules incubated with 1 mM glutamine. Conscious rats with chronic respiratory and chronic metabolic acidosis had similar arterial pHs (7.29 +/- 0.01 and 7.31 +/- 0.01), which were significantly lower than controls (7.41 +/- 0.04). NH3 production by kidneys from rats with chronic respiratory acidosis perfused at pH 7.4 did not differ significantly from normal controls (1.13 +/- 0.13 vs. 1.07 +/- 0.17 mumol X min-1 X g-1). By contrast, kidneys from rats with chronic metabolic acidosis produced significantly more NH3 than both these groups (2.73 +/- 0.29 mumol X min-1 X g-1). Cortical tubules from rats with chronic respiratory acidosis also showed no evidence of adaptation in both NH3 (8.8 +/- 0.8 vs. 11.6 +/- 0.8 mumol X min-1 X g-1) and glucose (1.38 +/- 0.08 vs. 1.41 +/- 0.13 mumol X min-1 X g-1) production in comparison with controls, whereas chronic metabolic acidosis stimulated both ammoniagenesis and gluconeogenesis twofold or more. Thus a low systemic pH does not account for the adaptation in the capacity of the kidney to produce either ammonia or glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

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