Gill morphology during hypercapnia in brown bullhead (Ictalurus nebulosus): role of chloride cells and pavement cells in acid‐base regulation

The role of gill chloride cells (CCs) and pavement cells (PVCs) in acid‐base regulation was evaluated in brown bullhead catfish ( Ictalurus nebulosus ) subjected to acute hypercapnia (water Pco 2 =15 torr). Chronic (10 day) cortisol treatment was used as a tool to cause CC proliferation to permit a comparison of the regulatory capacities in groups of fish with widely different gill CC populations. Cortisol (4mg kg −1 day −1 ) caused a pronounced increase (170%) in the surface area of CCs exposed to the water based on scanning and transmission electron microscope analysis. The density of PVC apical membrane microvilli was significantly increased (20%) by cortisol treatment. Exposure of either group of fish to hypercapnia caused similar changes in gill epithelial morphology including: (i) a marked reduction in the surface area of exposed CCs (52 and 78% reduction in the control and cortisol‐treated fish, respectively); and (ii) pronounced increases in PVC apical membrane microvilli density (21 and 27% in the control and cortisol‐treated fish, respectively). The rates of Cl − uptake (J in cl − ) and Na + uptake (J in Na + ) were elevated (150 and 262%, respectively) in the cortisol‐treated fish. Regardless of treatment, J in cl − was markedly reduced to approximately the same levels after 6 h of hypercapnia, J in Na + was stimulated in the control group and reduced in the cortisol‐treated group and thus, after 6 h of hypercapnia, J in Na + was equal in each group. The similar morphological responses in fish possessing different initial populations suggests that the predominant mechanism of acid‐base regulation during hypercapnia, reduction of C1 − /HCO 3 − exchange, is accomplished by removal of the CC‐associated C1‐/HCO 3 − exchange sites from the water. The increase in PVC microvilli density during hypercapnia suggests a role for the PVC in acid‐base regulation.