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 P(CO2) = 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 (4 mg 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 Cl- /HCO3- exchange, is accomplished by removal of the CC-associated Cl-/HCO3- exchange sites from the water. The increase in PVC microvilli density during hypercapnia suggests a role for the PVC in acid-base regulation.