The present study investigated acid–base regulatory mechanisms in seawater-acclimated green crabs (Carcinus maenas (L., 1758)). In full-strength seawater, green crabs are osmoconformers so that the majority of the observed responses were attributed to ion fluxes based on acid–base compensatory responses alone. Similar to observations in brackish-water-acclimated C. maenas, seawater-acclimated green crabs exposed to hypercapnia rapidly accumulated HCO3− in their hemolymph, compensating for the respiratory acidosis caused by excess hemolymph pCO2. A full recovery from the decreased hemolymph pH after 48 h, however, was not observed. Gill perfusion experiments on anterior gill No. 5 indicated the involvement of all investigated genes (i.e., bicarbonate transporters, V-(H+)-ATPase, Na+/K+-ATPase, K+-channels, Na+/H+-exchanger, and carbonic anhydrase) in the excretion of acid–base equivalents. The most significant effects were observed when targeting a potentially cytoplasmic and (or) basolaterally localized V-(H+)-ATPase, as well as potentially basolaterally localized bicarbonate transporter (likely a Na+/HCO3−-cotransporter). In both cases, H+ accumulated in the hemolymph and CO2 excretion across the gill epithelium was significantly reduced or even reversed when blocking bicarbonate transporters. Based on the findings in this study, a working model for acid–base regulatory mechanisms and their link to ammonia excretion in the gill epithelium of C. maenas has been developed.
Hypoxia attenuate ionic transport in the isolated gill epithelium of Carcinus maenas
