AbstractThe effect of hypercapnia on the acid‐base balance and acid‐equivalent transfers has been measured in the dogfishSqualus acanthias. Previous reports onSqualusare not in agreement as to the role played by compensatory acid‐base transfers between the animal and the water during hypercapnia.Cannulated animals were maintained in a closed circuit, seawater recirculation system. Plasma pH, Cco2(from which Pco2and [HCO3−] were calculated), and transfers of NH4+and HCO3−‐equivalent ions between the fish and the water, were measured during 24 hours of hypercapnic exposure (Pco2: 8–10 torr) and a subsequent 8–24 hour normocapnic recovery period.Respiratory acidosis resulted in a plasma pH depression, which was then almost completely compensated (within ˜ 0.1 pH unit) over 24 hours by a ˜ 20 mM increase in plasma [HCO3]. In contrast to previous studies on elasmobranch acid‐base regulation, hypercapnia induced a rapid 3 × increase in not only HCO3−‐equivalent uptake but also branchial ammonia (NH4+) excretion. These transfers combined for a net Δ H+loss to the water of 5.5 mmol kg−1. During the normocapnic period, net Δ H+was reversed to −6.9 mmol kg−1, nearly completely due to HCO3‐efflux.Several lines of evidence point to the contribution of gill Na+/NH4+exchange to the total ammonia excreted during hypercapnia, whereas NH3diffusion predominates during the recovery period. Likewise, Cl−/HCO3−or Cl−/OH−exchange may enh