Abstract

Background: In many cell types, basolateral K+ channels are important in maintaining transepithelial Na+ absorption and regulatory volume decrease (RVD) after hyposmolar stress. However, in the esophagus the effect of K+ transport in maintaining baseline short-circuit current (SCC) (Na+ absorption) and RVD is unknown. Methods: Ussing chambers were used to evaluate changes in SCC of rabbit esophageal mucosa in response to serosal Ba2+ (4 mmol/L), quinine (1 mmol/L), and increasing serosal [K+]. To determine whether K+ channel(s) are activated in RVD, changes in SCC in response to serosal hyposmolarity (156 mOsm) were assessed in the presence or absence of serosal quinine. Results: Serosal Ba2+, quinine, or increased serosal [K+] caused a decline in baseline SCC. Serosal hyposmolarity caused an increase in SCC that was not blocked by mucosal application of amiloride (10−4 mmol/L). In contrast, serosal quinine completely blocked the hyposmolar-induced increase in SCC. Conclusions: These studies suggest that rabbit esophageal cells possess Ba2+- and quinine-sensitive basolateral K+ channel(s) that are active under baseline conditions. Potassium conductance(s) also appear to be activated by external serosal hyposmolarity and may be involved in the process of RVD.

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