Further evidence for the regulation of the tight junction ion selectivity by cAMP in goldfish intestinal mucosa
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Summary
It has been reported that cAMP controls the transepithelial Cl− conductance in fish intestine (Bakker, R., Groot, J.A., 1984,Am. J. Physiol.246:G213–G217; Krasny, E.J., Madara, J.L., DiBona, D.L., Frizzell, R.A., 1983,Fed. Proc.42:1100). In both studies, the cAMP effect was interpreted as an increase in tight junction Cl− conductance, because cAMP did not change the membrane potential or membrane resistance ratio. However, the activation of a Cl− conductance in the membranes of a subset of the epithelial cells might be difficult to discern from an increase in tight junction Cl− conductance. Here we report experiments that were designed to distinguish a tight junction Cl− conductance from a membrane Cl− conductance in a subpopulation of the epithelial cells. The effect of hypotonicity on the cAMP-induced increase in transepithelial conductance showed that cAMP-induced conductance is located in series with the lateral intercellular spaces. Transepithelial serosa to mucosa direct current caused an increase in resistance due to so-called transport number effects. Forskolin abolished the transport number effects, indicating that cAMP increases the Cl− conductance of the tight junctions. Increasing cAMP did not change mannitol fluxes, whereas Cl− fluxes more than doubled. Changes in dilution potential and transepithelial resistance demonstrated that the cAMP-induced conductance is specific for Cl− and Br− as opposed to I−, NO 3 − , SO 4 2− and gluconate−. In contranst, cytochalasin D also decreased the transepithelial resistance and dilution potential in Nagluconate Ringer's. This demonstrates that cAMP acts on the tight junctions in a more specific manner than cytochalasin D.
Key Words
chloride permeability cyclic AMP cytochalasin D intestine ion selectivity leaky epithelia tight junctions transport number effectsPreview
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References
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