Physiological and morphological regulation of acid–base status during hypercapnia in rainbow trout (Oncorhynchus mykiss)

A kinetic analysis (Michaelis constant (Km) and maximal flux (Jmax)) of the branchial Na+ and Cl− influx mechanisms, along with measurements of blood total CO2 content [Formula: see text], net acidic–basic equivalent fluxes, and gill chloride cell morphology, was performed using rainbow trout (Oncorhynchus mykiss) before, during, and after 96 h exposure to environmental hypercapnia (water [Formula: see text]; 1 torr = 133.3 kPa). Exposure to hypercapnia caused (i) a net acidic equivalent loss (negative [Formula: see text]) that was accounted for entirely by reductions in titratable alkalinity flux (JTA), (ii) an increase in [Formula: see text] from 8.4 ± 0.5 to 20.7 ± 0.4 mmol/L, and (iii) no alteration either in [Formula: see text], [Formula: see text], or [Formula: see text]; [Formula: see text] increased (affinity was reduced). Chloride cell fractional area was reduced by 40% from 174 250 ± 15 650 μm2/mm2 under control conditions to 104 329 ± 17 991 μm2/mm2 after 96 h of hypercapnia. In the posthypercapnic period, there was (i) a net acidic equivalent gain (positive [Formula: see text]) that was accounted for entirely by an elevation in JTA, (ii) a rapid reduction of blood [Formula: see text], (iii) an increase of chloride cell fractional area to control values (179 105 ± 35 233μm2/mm2), and (iv) increases and decreases in [Formula: see text] (564 ± 50 versus 224 ± 21 μmol∙kg−1∙h−1 in the prehypercapnic period) and [Formula: see text] (381 ± 85 versus 585 ± 92 μmol∙kg−1∙h−1), respectively. The results suggest that morphological alteration of the gill chloride cell fractional area is an important response to acid–base disturbances. The results are discussed with respect to the relative roles of morphological alteration of gill chloride cell fractional area and variation in internal substrate (HCO3−) in modifying branchial Cl−/HCO3− exchange for acid–base regulation.