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) −[Formula: see text]] and net H+ excretion became negative (net base excretion) with unchanged [Formula: see text] efflux. During RA, urine pH did not change, but net H+ excretion increased as a result of a modest rise in [Formula: see text] and substantial elevation in [TA −[Formula: see text]] 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 −[Formula: see text]] and a smaller elevation in phosphate but a sevenfold greater increase in[Formula: see text] efflux. In urine samples of the same pH, [TA − [Formula: see text]] was greater during RA (reflecting phosphate secretion), and[Formula: see text] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, α-ketoglutarate dehydrogenase, alanine aminotransferase, phospho enolpyruvate 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.
The kinetics of inorganic phosphate excretion in the acidotic rabbit during intravenous phosphate loading: a pseudo-ruminant model