Carbonic anhydrase expression in the branchial ionocytes of rainbow trout

摘要

Rainbow trout (Oncorhynchus mykiss) exposed to acid-base challenges activate branchial mechanisms for the excretion of acid-base equivalents. Current models of branchial acid-base excretion in freshwater rainbow trout propose two main ionocyte types: the peanut lectin agglutinin-positive (PNA(+)) mitochondrion-rich cell or ionocyte is believed to secrete HCO3- in exchange for Cl-, whereas H+ secretion is thought to occur across PNA(-) ionocytes in exchange for Na+. Both HCO3- and H+ are supplied by intracellular hydration of CO2 catalysed by cytosolic carbonic anhydrase (CAc). Immunohistochemical approaches revealed that under control conditions, CAc was detectable in 92.3 +/- 1.0% (N=11) of PNA(-) ionocytes, and the abundance of PNA(-) ionocytes increased in response to systemic acidosis elicited by 72 h exposure to water of low pH (nominally pH 4.5), hypercapnia (1% CO2, nominally 7.6 Torr) or hyperoxia (achieved by gassing water with pure O-2), as did the abundance of PNA(-) ionocytes that exhibited immunofluorescence for CAc. However, just 4.3 +/- 0.6% (N=11) of PNA+ ionocytes expressed detectable CAc under control conditions. Marked increases in the abundance of CAc-positive PNA(+) ionocytes were detected following exposure of trout to a base load via recovery from hypercapnia or base infusion (72 h infusion with 140 mmol l(-1) NaHCO3). The percentage of CAc-positive PNA+ ionocytes also was increased in trout treated with cortisol (10 mg kg(-1) hydrocortisone 21-hemisuccinate daily for 7 days). These results suggest that regulation of CA within PNA(+) ionocytes and/or the abundance of CAc-positive PNA(+) ionocytes plays a role in activating base secretion in response to systemic alkalosis.