Fish gill carbonic anhydrase: acid-base regulation or salt transport?
During the passage of blood through the fish gill, large oscillations in oxygen and carbon dioxide content occur. Although the increase in oxygen content is related to oxygen binding by red blood cells, the fall in carbon dioxide content is independent of red blood cells and their complement of carbonic anhydrase. This loss of venous carbon dioxide content is primarily the result of the movement of plasma bicarbonate into the gill epithelium, where it subsequently can be converted to molecular carbon dioxide by branchial carbonic anhydrase. The ultimate control of the bicarbonate flux and hence plasma hydrogen ion regulation is coupled to salt movements also occurring in the fish gill. This evidence in conjunction with carbonic anhydrase localization studies makes it possible to formulate a model capable of explaining acid-base regulation as well as salt transport in freshwater- or seawater-adapted fish. In light of this model the role of the "chloride cell" is discussed.
D000136:Acid-Base Equilibrium; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001693:Biological Transport, Active; D002245:Carbon Dioxide / Q000378:metabolism; D002256:Carbonic Anhydrases / Q000378:metabolism*; D005399:Fishes / Q000378:metabolism*; D005880:Gills / Q000201:enzymology*; D010101:Oxygen Consumption
D001639:Bicarbonates; D002245:Carbon Dioxide; D002256:Carbonic Anhydrases