Localization of cAMP‐ and aldosterone‐induced K<sup>+</sup> secretion in rat distal colon by conductance scanning

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<jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>Aldosterone‐ and adrenaline‐induced K<jats:sup>+</jats:sup> secretion were investigated in rat late distal colon using conductance scanning and Ussing chamber techniques. K<jats:sup>+</jats:sup> secretion was unmasked by the K<jats:sup>+</jats:sup> channel blocker tetraethylammonium (TEA). Electrogenic Na<jats:sup>+</jats:sup> absorption was inhibited by amiloride. Rb<jats:sup>+</jats:sup> net fluxes consistently measured about 80 % of K<jats:sup>+</jats:sup> secretion estimated using change in short‐circuit current (Δ<jats:italic>I</jats:italic><jats:sub>SC</jats:sub>) measurements.</jats:p></jats:list-item> <jats:list-item><jats:p>Partial block of K<jats:sup>+</jats:sup> absorption by mucosal ouabain did not change TEA‐sensitive K<jats:sup>+</jats:sup> secretion. Thus, K<jats:sup>+</jats:sup> absorption and K<jats:sup>+</jats:sup> secretion are not coupled.</jats:p></jats:list-item> <jats:list-item><jats:p>Additivity of Rb<jats:sup>+</jats:sup> fluxes as well as Δ<jats:italic>I</jats:italic><jats:sub>SC</jats:sub> caused by 3 nM aldosterone (6 h <jats:italic>in vitro</jats:italic> incubation) and, subsequently, adrenaline suggested additivity of aldosterone‐induced and cAMP‐mediated K<jats:sup>+</jats:sup> secretion in the presence of amiloride.</jats:p></jats:list-item> <jats:list-item><jats:p>Conductance scanning under control conditions revealed a small TEA‐sensitive K<jats:sup>+</jats:sup> conductivity in surface epithelium (0.3 ± 0.2 mS cm<jats:sup>−2</jats:sup>) but not in crypts, as well as a small basal K<jats:sup>+</jats:sup> secretion in surface epithelium (Δ<jats:italic>I</jats:italic><jats:sub>SC</jats:sub>= 0.3 μ<jats:sc>m</jats:sc>ol h<jats:sup>−1</jats:sup> cm<jats:sup>−2</jats:sup>), which increased during sham incubation.</jats:p></jats:list-item> <jats:list-item><jats:p>Aldosterone (3 nM, 6 h <jats:italic>in vitro</jats:italic> incubation) resulted, after correction for the basal K<jats:sup>+</jats:sup> secretion, in a K<jats:sup>+</jats:sup> secretion of Δ<jats:italic>I</jats:italic><jats:sub>SC</jats:sub>= 0.9 μ<jats:sc>m</jats:sc>ol h<jats:sup>−1</jats:sup> cm<jats:sup>−2</jats:sup>. Aldosterone induced a TEA‐sensitive conductivity of 1.1 ± 0.3 mS cm<jats:sup>−2</jats:sup> in surface epithelium, but not in crypts.</jats:p></jats:list-item> <jats:list-item><jats:p>Adrenaline (5 μ<jats:sc>m</jats:sc>) caused, in fresh tissue, a K<jats:sup>+</jats:sup> secretion of Δ<jats:italic>I</jats:italic><jats:sub>SC</jats:sub>= 1.2 μ<jats:sc>m</jats:sc>ol h<jats:sup>−1</jats:sup> cm<jats:sup>−2</jats:sup> and equal conductivity changes in crypts (0.7 ± 0.2 mS cm<jats:sup>−2</jats:sup>) and surface epithelium (0.7 ± 0.1 mS cm<jats:sup>−2</jats:sup>).</jats:p></jats:list-item> <jats:list-item><jats:p>We conclude that K<jats:sup>+</jats:sup> secretion induced by aldosterone in physiological concentration is restricted to surface epithelium, whereas cAMP‐mediated K<jats:sup>+</jats:sup> secretion is located equally in crypts and surface epithelium.</jats:p></jats:list-item> </jats:list> </jats:p>

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