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

1095-8649

Blackwell Publishing Journal Backfiles 1879-2005

Biology

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.

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