Renal responses of trout to chronic respiratory and metabolic acidoses andmetabolic alkalosis

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO3 inf usion for 48 h were used to create chronic respiratory (RA) or metabolic ac idosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alka losis, urine pH increased, and [titratable acidity (TA) - HCO3-] and net H excretion became negative (net base excretion) with unchanged NH4+ efflux. During RA, urine pH did not change, but net H+ excretion increased as a re sult of a modest rise in NH4+ and substantial elevation in [TA - HCO3-] eff lux accompanied by a large increase in inorganic phosphate excretion. Howev er, during MA, urine pH fell, and net H+ excretion was 3.3-fold greater tha n during RA, reflecting a similar increase in [TA - HCO3-] and a smaller el evation in phosphate but a sevenfold greater increase in NH4+ efflux. In ur ine samples of the same pH, [TA - HCO3-] was greater during RA (reflecting phosphate secretion), and [NH4+] was greater during MA (reflecting renal am moniagenesis). Renal activities of potential ammoniagenic enzymes (phosphat e-dependent glutaminase, glutamate dehydrogenase, cl-ketoglutarate dehydrog enase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and pla sma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only al anine aminotransferase increased. The differential responses to RA vs. MA p arallel those in mammals; in fish they may be keyed to activation of phosph ate secretion by RA and cortisol mobilization by MA.