AREGU August 46/2

Wood, Chris M., C. Louise Milligan, and Patrick J. Walsh. Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R482–R492, 1999.—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) 2 HCO3 ] and net H1 excretion became negative (net base excretion) with unchanged NH4 1 efflux. During RA, urine pH did not change, but net H1 excretion increased as a result of a modest rise in NH4 1 and substantial elevation in [TA 2 HCO3 ] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H1 excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA 2 HCO3 ] and a smaller elevation in phosphate but a sevenfold greater increase in NH4 1 efflux. In urine samples of the same pH, [TA 2 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.