Cyclic AMP stimulation of Cl− secretion by the opercular epithelium: The basolateral chloride uptake mechanism

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Abstract
The isolated, short‐circuited opercular epithelium of Fundulus heteroclitus, secretes Cl− by a mechanism dependent on the presence of serosal Na+ and inhibited by bumetanide and furosemide. Under serosal Na+‐free conditions the active Cl− secretion is abolished. However, subsequent elevations of intracellular cyclic AMP (cAMP) levels with isoproterenol or forskolin stimulated Cl− secretion markedly. This stimulation was unaffected by SITS, DIDS, methazolamide, and HCO−3‐free solutions, but was blocked by furosemide and bumetanide. Determinations of relative intracellular 36Cl− levels showed a Na+ dependence of intracellular 36Cl− in epithelia not stimulated by isoproterenol and a Na+ independence of intracellular 36Cl− in isoproterenol stimulated epithelia. In both conditions, the intracellular 36Cl− was bumetanide sensitive. The results indicate that cAMP stimulation of Cl− secretion can occur by a Na+‐independent, loop diuretic‐inhibitable mechanism, which may be operative even in the presence of Na+. Whether this is a separate Cl− uptake mechanism or a cAMP‐induced alteration in the normal Na+‐dependent mechanism could not be determined. In either instance, an alternative to the Na+ gradient as a source of energy for Cl− uptake into the cell across the basolateral membrane is required.