Krick W, Dölle A, Hagos Y, Burckhardt G
Abteilung Vegetative Physiologie und Pathophysiologie, Zentrum Physiologie und Pathophysiologie, Humboldtallee 23, D-37073 Göttingen, Germany.
Pflugers Arch. 1998 Feb;435(3):415-21. doi: 10.1007/s004240050532.
The chloride conductance in brush-border membrane vesicles prepared from pig kidney cortex was investigated using a light-scattering assay, anion-diffusion-potential-dependent Na+-D-glucose cotransport and 36Cl- influx. K+-diffusion-potential-driven salt exit from, or entry into, the vesicles was slow in the presence of gluconate, SO42- and F-, intermediate with Cl- and Br-, and fast with I-, NO3-, and SCN-. Stimulation of Na+-D-glucose uptake followed a similar anion sequence. Conductive Cl- flux had a low activation energy and was inhibited by suphhydryl reagents, the stilbene disulphonates 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate (SITS) and 4, 4'-diisothiocyanato-2,2'-disulphonate (DIDS), and the arylaminobenzoates diphenylamine-2-carboxylic acid (DPC) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). Intravesicular Ca2+ and extravesicular nucleotides were without effect on conductive Cl- flux. These characteristics tentatively exclude some known Cl- channels and leave members of the ClC family as possible candidates responsible for the Cl- conductance in brush-border membranes.
