Hypercapnic acidosis in the rainbow trout (Salmo gairdneri). II. Renal ionic fluxes

Abstract

The involvement of the rainbow trout kidney in acid-base regulation was assessed before, during, and after 72 h of exposure to external hypercapnia (1% CO2). Hypercapnia caused a significant elevation of renal acid excretion throughtout most of the hypercapnic period, which could account for 16% of the overall compensatory increase in the plasma bicarbonate concentration. The two predominant urine buffers, phosphate and ammonia, both increased markedly during hypercapnia, thereby preventing reductions in urine pH during the period of enhanced urinary acidification. Stimulation of tubular H+ secretion was the mechanism responsible for the elevation of acid excretion and, more importantly, ensured tubular reabsorpiton of the additional HCO3- that must have appeared in the glomerular filtrate. Such a mechanism is considered essential for the ultimate compensation of hypercapnia acidosis. The results are discussed with respect to the possible involvement of increased plasma epinephrine levels in mediating the various renal responses of hypercapnic acidosis.