Wood, C.M., Milligan, C.L. & Walsh, P.J. (1999). Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis. Am. J. Physiol. 277:R1415-R1426.
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) - HCO3-] and net H+ excretion became negative (net base excretion)
wit unchanged NH4+ efflux. During RA, urine pH did not change,
but net H+ excretion increased as a result of a modest rise in
NH4+ and substantial elevation in [TA-HCO3-] 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-HCO3-] and
a smaller elevation in phosphate but a sevenfold greater increase
in NH4+ efflux. In urine samples of the same pH, [TA-HCO3-] was
greater during RA (reflecting phosphate secretion) and [NH4+]
was greater during MA (reflecting renal ammoniagenesis). Renal
activities of potential ammoniagenic enzymes (phosphate-dependent
glutaminase, glutamate dehydrogenase, a-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.