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 Pco2=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 (Jincl−) and Na+ uptake (JinNa+) were elevated (150 and 262%, respectively) in the cortisol‐treated fish. Regardless of treatment, Jincl− was markedly reduced to approximately the same levels after 6 h of hypercapnia, JinNa+ was stimulated in the control group and reduced in the cortisol‐treated group and thus, after 6 h of hypercapnia, JinNa+ 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−/HCO3− exchange, is accomplished by removal of the CC‐associated C1‐/HCO3− exchange sites from the water. The increase in PVC microvilli density during hypercapnia suggests a role for the PVC in acid‐base regulation.