Branchial solute fluxes as well as blood respiratory, ionic, and acid–base variables were monitored before, during, and after 72 h of exposure to external hypercapnia (1% CO2; [Formula: see text]). Hypercapnia induced an immediate extracellular respiratory acidosis that was gradually regulated over the 72-h period by an elevation of the plasma bicarbonate [Formula: see text] level. Red blood cell pH changed in a manner similar to whole blood pH but the reduction of red blood cell pH during hypercapnia was significantly less than that predicted from in vitro experiments. We argue that elevated plasma levels of epinephrine in the first 12 h of hypercapnia may serve to stabilize red blood cell pH during the severe reduction of whole blood pH, thereby preventing excessive depressions of arterial oxygen content. Elevated external CO2 tension caused changes in the branchial net flux (JnetCl−) such that the arithmetic difference between sodium net flux (JnetNa+) and JnetCl− (JnetNa+ – JnetCl−) increased during hypercapnia and then decreased post-hypercapnia. These results are consistent with enhanced branchial acid excretion and are discussed with reference to the involvement of the gill in the regulation of hypercapnic acidosis.

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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 throughout most of the hypercapnic period, which could account for 16% of the overall compensatory increase in 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 reabsorption of the additional [Formula: see text] that must have appeared in the glomerular filtrate. Such a mechanism is considered essential for the ultimate compensation of hypercapnic 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.

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