Abstract

ALTHOUGH it has been generally assumed that marine teleost fish balance the net influx of NaCl (from diffusional gain and oral ingestion of seawater) by active extrusion of both ions1–3, the proposition of active extrusion of Na has been questioned. It has been shown4–11 that marine teleosts generally maintain a transepithelial potential (t.e.p.) in the range +10−+25 mV (blood relative to seawater), which is nearly equal to that which could nullify the Na concentration gradient between the teleost and seawater. Thus, it has been suggested that Na is maintained in electrochemical equilibrium across the teleost gill and only Cl is actively extruded4,6–8,12. The Na efflux changes accompanying rapid changes in external Na or K concentrations have been used to support a model of both Na–Na and Na–K exchanges13–16, and have been shown to result at least partially from changes in the t.e.p. (refs 7–9, 12) rather than uncoupling of ionic exchange systems. Histochemical localisation of the Na–K-activated ATPase in teleost gill tissue indicates that it is predominantly basal rather than apical17,18. This suggests that the enzyme may be involved in gill cell volume regulation rather than transepithelial extrusion of Na.

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