Relationships between branchial chloride cells and gas transfer in freshwater fish.

The gill lamellar epithelium is composed of two predominant cell types, pavement cells and mitochondria-rich chloride cells. The chloride cells play a vital role in ionic regulation because they are the sites of Ca2+ and Cl- uptake from water. Consequently, lamellar chloride cell proliferation occurs in response to ionoregulatory challenges so as to increase the ion-transporting capacity of the gill. It has been argued that such chloride cell proliferation might increase the thickness of the blood-to-water diffusion barrier and thereby impede gas diffusion. This review focuses on the potential negative consequences of chloride cell proliferation on gas transfer and possible compensatory mechanisms that might minimise the extent of respiratory impairment. Two approaches were used to evoke chloride cell proliferation in rainbow trout, hormone treatment (growth hormone/cortisol) and exposure to soft water. In all cases, chloride cell proliferation was associated with a pronounced thickening of the lamellar diffusion barrier. The thickening of the diffusion barrier was associated with a significant impairment of gas transfer. Subsequent studies revealed that several compensatory physiological responses occurred concurrently with the chloride cell proliferation to alleviate or reduce the detrimental consequences of the thickened diffusion barrier. These included hyperventilation, an increased affinity of haemoglobin-oxygen binding and earlier onset of catecholamine release during acute hypoxia.