PHYSIOLOGICAL AND MORPHOLOGICAL REGULATION OF ACID-BASE STATUS DURING HYPERCAPNIA IN RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)

A kinetic analysis (Michaelis constant (K(m)) and maximal flux (J(max)) of the branchial Na+ and Cl- influx mechanisms, along with measurements of blood total CO2 content (Cco2), 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 PCO2 = 7.5 torr; 1 torr = 133.3 kPa). Exposure to hypercapnia caused (i) a net acidic equivalent loss (negative J(net)H+) that was accounted for entirely by reductions in titratable alkalinity flux (J(TA)), (ii) an increase in Cco2 from 8.4 +/- 0.5 to 20.7 +/- 0.4 mmol/L, and (iii) no alteration either in J(max)Na+, J(max)Cl-, or K(m)Na+; K(m)Cl- was increased (affinity was reduced). Chloride cell fractional area was reduced by 40% from 174 250 +/- 15 650 mum2/mm2 under control conditions to 104 329 +/- 17 991 mum2/mm2 after 96 h of hypercapnia. In the posthypercapnic period, there was (i) a net acidic equivalent gain (positive J(net)H+) that was accounted for entirely by an elevation in J(TA), (ii) a rapid reduction of blood Cco2, (iii) an increase of chloride cell fractional area to control values (179 105 +/- 35 233 mum2/mm2), and (iv) increases and decreases in J(max)Cl- (564 +/- 50 versus 224 +/- 21 mumol . kg-1 . h-1 in the prehypercapnic period) and J(max)Na+ (381 +/- 85 versus 585 +/- 92 mumol . 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.