CHOE, K*; EVANS, D: Compensation for Hypercapnia by a Euryhaline Elasmobranch in Fresh Water: roles of gills and kidneys

In fish, hypercapnia is compensated by increased acid excretion by gills and kidneys, with gills playing a larger role. Because gill acid excretion depends on external sodium, a fish’s ability to regulate pH decreases with salinity. Alternatively, the magnitude of kidney acid excretion seems to depend on urine flow rate, and therefore increases with decreasing salinity. For example, teleosts (advanced bony fish) in fresh water compensate their blood pH slower than teleosts in seawater even though their kidneys play a larger role. Acid-base regulation in freshwater elasmobranchs (sharks, skates and rays) has not been studied. Therefore, in one series, blood acid-base parameters and whole-animal net-acid efflux, were measured in freshwater Atlantic stingrays (Dasyatis sabina) during hypercapnia to determine the time course of compensation. In another series, urine net-acid excretion was measured to determine the quantitative roles of gills and kidneys. In the first series, each stingray was fitted with a blood cannula and placed in a flux chamber of fresh water. Blood pH, total CO₂, and whole-animal net-acid excretion were monitored before and during 1% hypercapnia. In a second series, each stingray was fitted with urinary catheters, and put through the same hypercapnia regime. Plasma pH decreased from 7.84 to 7.53 by 2 h and recovered to 7.62 by 24 h. Plasma [HCO₃^–] increased slowly from 6.79 to 10.39 mmol l^-1 by 24 h. This new bicarbonate was entirely from extra-renal sources (presumably gills) because there was always a slight net base loss in urine. Therefore, like teleosts, euryhaline elasmobranchs appear to compensate for hypercapnia slowly in fresh water. However, unlike in teleosts, the kidneys of this freshwater elasmobranch do not appear to respond to hypercapnia.