Rapid blood acid–base regulation by European sea bass (Dicentrarchus labrax) in response to sudden exposure to high environmental CO(2)

Fish in coastal ecosystems can be exposed to acute variations in CO(2) of between 0.2 and 1 kPa CO(2) (2000–10,000 µatm). Coping with this environmental challenge will depend on the ability to rapidly compensate for the internal acid–base disturbance caused by sudden exposure to high environmental CO(2) (blood and tissue acidosis); however, studies about the speed of acid–base regulatory responses in marine fish are scarce. We observed that upon sudden exposure to ∼1 kPa CO(2), European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ∼40 min, thus restoring haemoglobin–O(2) affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ∼2 h, which is one of the fastest acid–base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO(3)(−) in blood, which increased from ∼4 to ∼22 mmol l(−1). While the abundance and intracellular localisation of gill Na(+)/K(+)-ATPase (NKA) and Na(+)/H(+) exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid–base regulation was completely prevented when the same high CO(2) exposure occurred in seawater with experimentally reduced HCO(3)(−) and pH, probably because reduced environmental pH inhibited gill H(+) excretion via NHE3. The rapid and robust acid–base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO(2) fluctuations that naturally occur in coastal environments.