Abstract
It has widely been established that Cl − transport is defective in cystic fibrosis fibroblasts. In the present study, the effect of elevation of intracellular concentration of cyclic AMP and calcium on the efflux of Cl − from human fibroblasts has been investigated. Cyclic AMP analogs (8-bromo cAMP and dibutyryl cAMP) and a beta agonist (isoproterenol) induced only a weak stimulation (5–10%) of Cl − efflux. Conversely, elevation of cytoplasmic calcium concentration produced by addition of the Ca 2+ ionophore A23187 in the efflux medium, did not affect Cl − efflux. Our data indicate that the response of Cl − efflux to elevation of cAMP and calcium is similar in normal and cystic fibrosis fibroblasts. Exposure to hypotonic medium induced a significant stimulation of Cl − efflux in fibroblasts from both normal and cystic fibrosis individuals. Substitution of Cl − in the medium by gluconate and the subsequent addition of furosemide did not inhibit the effect of hypotonicity, indicating the involvement of a conductive pathway for Cl − transport, which was insensitive to oligomicin C.
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