Cl-absorption in European eel intestine and its regulation.

• Published in: Journal of Experimental Zoology
• Main Authors: SCHETTINO, Trifone, LIONETTO, Maria Giulia
• Other Authors: Schettino, Trifone, Lionetto, Maria Giulia
• Format: Article in Journal/Newspaper
• Language: English
• Published: 2003
• Subjects: Anguilla anguilla
• Online Access: http://hdl.handle.net/11587/300514; https://doi.org/10.1002/jez.a.10310

The intestinal epithelium of the euryhaline teleost fish, Anguilla anguilla, absorbs Cl-transepithelially. This gives rise to a negative transepithelial potential at the basolateral side of the epithelium and to a measured short circuit current. Cl- absorption occurs via bumetanide-sensitive Na+-K+-2Cl- cotransport, localized on the luminal membrane. The cotransport operates in parallel with a luminal K+ conductance that recycles the ion into the lumen. Cl- leaves the cell across the basolateral membrane by way of Cl- conductance and presumably via a KCl cotransport. The driving force for this process is provided by the electrochemical sodium gradient across the plasma membrane, generated and maintained by the basolateral Na+-K+-ATPase. The resulting NaCl absorption process is active and enables marine fish to take up water, thereby compensating for water that was lost passively from the body. Fresh water acclimatized eel also absorb Cl- actively, although in smaller quantities, utilizing the same ion transport mechanisms as marine eels. This mechanism is basically the same as the model proposed for the thick ascending limb (cTAL). Cl- absorption is regulated by a number of cellular factors, such as HCO3-, pH, Ca2+, cyclic nucleotides, and cytoskeletal elements. It is sensitive to osmotic stress, and therefore is a good physiological model to study ion transport mechanisms that are activated when osmotic stress induces cell volume regulation. The activation of these various ion transport pathways is dependent on cellular transduction mechanisms in which phosphorylation events (mainly by PKC and MLCK for the hypertonic response) and cytoskeletal elements, either microfilaments or microtubules, seem to play key roles.