Radioactive labelling of the CaCO3 in the crab's carapace was employed as a tool to study the contribution of the carapace carbonates to acute buffering of acid-base disturbances. Since Ca2+ uptake is extremely rapid during the post-moult period, crabs that moulted in the laboratory were incubated with 45Ca for 5 days immediately following the moult in order thoroughly to load the carapace carbonate pool with radiolabel. After a subsequent 2-week interval for feeding and completion of the post-moult carapace mineralization phase, these 45Ca-loaded crabs were subjected to a 24h control period and a 24h hypercapnic period (water equilibrated with 2 % CO2 in air) to induce an internal acidosis. Compared with the control period, a compensatory increase in [HCO3] of 17 mequiv1−1 was observed in the blood, along with an apparent H+ excretion to the external sea water of 10.8 mequiv kg−1. A statistically significant increase in circulating [Ca2+] and in the specific radioactivity of the blood Ca2+ reached a maximum during the first 3 h of the compensatory phase. By measuring the radioactivity appearing in the water and the blood, and the specific radioactivity of the carapace carbonates, the contribution of the carapace carbonates was calculated to be 7.5% of the total compensatory H+ disposal. The rapid exchange of Ca2+ with the external medium, coupled with physiological regulation of blood [Ca2+] minimized changes in blood [Ca2+]. The total dissolution of carapace CaCO3 was approximately 0.9 mequiv kg−1, less than 0.1% of the quantity contained in the shell. The carapace carbonates, therefore, do contribute to acute buffering of hypercapnic acidosis, but their quantitative importance is small, with the gills serving to conduct most of the compensatory exchanges with the environment.

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