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1 Department of Biology,
Exposure to
hyperoxia (500-600 torr) or low pH (4.5) for 72 h or
NaHCO3 infusion for 48 h were used
to create chronic respiratory (RA) or metabolic acidosis (MA) or
metabolic alkalosis in freshwater rainbow trout. During alkalosis,
urine pH increased, and [titratable acidity (TA)
HCO
3] and net
H+ excretion became negative (net
base excretion) with unchanged NH+4 efflux.
During RA, urine pH did not change, but net
H+ excretion increased as a result
of a modest rise in NH+4 and substantial
elevation in [TA
HCO
3] efflux accompanied by a
large increase in inorganic phosphate excretion. However, during MA,
urine pH fell, and net H+
excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA
HCO
3] and a smaller elevation in
phosphate but a sevenfold greater increase in
NH+4 efflux. In urine samples of the same pH,
[TA
HCO
3] was
greater during RA (reflecting phosphate secretion), and
[NH+4] was greater during MA
(reflecting renal ammoniagenesis). Renal activities of potential
ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate
dehydrogenase,
-ketoglutarate dehydrogenase, alanine
aminotransferase, phosphoenolpyruvate carboxykinase) and plasma
levels of cortisol, phosphate, ammonia, and most amino acids (including
glutamine and alanine) increased during MA but not during RA, when only
alanine aminotransferase increased. The differential responses to RA
vs. MA parallel those in mammals; in fish they may be keyed to
activation of phosphate secretion by RA and cortisol mobilization by MA.
renal ammoniagenesis; phosphate; titratable acidity; glutamine; cortisol
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