Acid-base balance and ion transfers were studied in the carp, Cyprinus carpio L., during and after 48 h of exposure to environmental hypercapnia (PCOCO27.5 Torr). Plasma pH, PCOCO2, [HCO3], and net transfers of HCO3, NH4+, Cl and Na+ between the fish and the environmental water were measured periodically throughout the experiment.

Over the first 8 h of hypercapnia, plasma PCOCO2 increased by 7.6 Torr with a concurrent decrease in plasma pH of 0.28 units. Plasma [HCO3] was slowly elevated from about 14 to 22 mM after 48 h, at which point 50% of the pH depression expected at constant bicarbonate concentration had been compensated. The net amount of H+ transferred to the water was 3.3 mmol kg−1 fish, representing a 115% increase in the rate of cumulative H+ efflux, and inducing an elevation of both intracellular and extracellular [HCO3]. Cl transfer was reversed from a net uptake to a net efflux, while net Na+ influx was increased slightly.

Following hypercapnia, plasma pH returned to control values within 1 h, while the plasma [HCO3], which was elevated during hypercapnia, fell continuously to reattain pre-hypercapnic control values after 20 h. The [HCO3] decrease was due to the net gain of H+ ions from the water during this period. Cl transfer returned to a net uptake, while the original Na+ influx was reversed to a net loss.

Acid-base regulatory responses in the carp are qualitatively similar to those observed in other fish, though the time required for compensatory pH adjustment is longer. It is concluded that alterations in the rates of Cl/HCO3 and Na+/H+ exchanges during hypercapnia and Na+/H+ exchange following hypercapnia, play a significant role in the compensation of respiratory acid-base disturbances in these animals.

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