European eels were exposed for 6 weeks to water CO(2) partial pressures (P(CO)(2)) from ambient (approx. 0.8 mmHg), through 15+/-1 mmHg and 30+/-1 mmHg to 45+/-1 mmHg in water with a total hardness of 240 mg l(-1) as CaCO(3), pH 8.2, at 23+/-1 degrees C. Arterial plasma P(CO)(2) equilibrated at approximately 2 mmHg above water P(CO)(2) in all groups, and plasma bicarbonate accumulated up to 72 mmol l(-1) in the group at a water P(CO)(2) of 45 mmHg. This was associated with an equimolar loss of plasma Cl(-), which declined to 71 mmol l(-1) at the highest water P(CO)(2). Despite this, extracellular acid-base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O(2) content (Ca(O)(2)), of progressive severity with increasing P(CO)(2). All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although Ca(O)(2) was reduced by approximately 50% at the highest P(CO)(2), there was no effect of hypercapnia on the eels' tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl(-) levels while compensating tissue intracellular pH, and which can meet the O(2) requirements of routine and active metabolism despite profound hypoxaemia.