The role of K+ and Cl− conductances in chloride secretion by the opercular epithelium

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Abstract
The opercular epithelium of the teleost Fundulus heteroclitus, when mounted in a lucite chamber under short-circuited conditions, secretes Cl− at a rate equivalent to the short-circuit current (Isc). The transepithelial Na+ movements are passive and proceed by a paracellular pathway. The addition of 2 × 10−3 M Ba2+ to the serosal bathing solution inhibited the Isc 76.8% with no effect on the transepithelial conductance (Gt). The addition of 5 × 10−4 M Cu2+ to the mucosal bathing solution inhibited the Isc 79.6% and reduced the Gt 35.6%. These inhibitory effects of Ba2+ and Cu2+ on the Isc were initiated within 1 minute after exposure with maximum effects occurring within 20 and 30 minutes, respectively. Simultaneous 36Cl− and 22Na+ unidirectional fluxes were performed on paired epithelia from the same fish. Serosal Ba2+ and mucosal Cu2+ inhibited the Cl− secretory flux 30.2 and 58.9%, respectively. The resulting net Cl− flux after inhibition was not significantly different from the mean measured Isc. Neither ion had significant effects on the Cl− influx (mucosa to serosa) or the unidirectional Na fluxes. These results indicated that the effects of both Ba2+ and Cu2+ were most likely exclusive to the transcellular Cl− pathway. Ba2+ is proposed to inhibit Cl− secretion by blocking the basolateral K+ channels, depolarizing the cell, and reducing the electrochemical driving force for Cl− across the apical membrane. Cu2+ is proposed to inhibit Cl− secretion by blocking the apical membrane Cl− channels. The results are in keeping with the proposed mechanism for Cl− secretion by indicating that the Cl− exit step across the apical membrane occurs via Cl− conductive channels and is driven passively by a favorable electrical gradient.