In calcium-transporting epithelia, calcium can move transcellularly (when it passes inwards, from mucosa to serosa) and paracellularly (when it moves in both an inward and outward direction). An epithelium is considered to be ‘tight’ when the transcellular route dominates and leaky when there is additional significant paracellular transport. The branchial epithelium of the gills of freshwater fish is a good model for tight epithelia, whereas the gills of seawater fish and the intestine present a model for leaky epithelia. Generally, the regulation of transcellular inward calcium transport determines whether net absorption occurs and the regulation of paracellular calcium transport is pivotal to secretion in calcium-transporting epithelia. In its simplest form, transcellular transport requires movement of Ca2+ across the apical membrane, through the cytosol and across the basolateral membrane. At the same time, cellular calcium homeostasis must be maintained and, to this end, calcium is buffered in the cytosol by calcium-binding proteins and sequestered in the endoplasmic reticulum and mitochondria. Movement of calcium from the exterior of the cell to the cytosol is passive, down an electrochemical gradient, and appears to be regulated through channel or carrier proteins. The apical membrane contains a hormone-regulated carrier mechanism for Ca2+ entry. Movement from the cytosol to the exterior requires energy-consuming extrusion mechanisms, involving Ca2+-ATPase and/or Na+/Ca2+ exchange. The roles of such mechanisms in calcium transport phenomena in fish gills and intestine will be addressed.

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