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.
