title: Hypotonic shock activated Cl- and K+ pathways in human fibroblasts.
abstract: The exposure of human fibroblasts to hypotonic medium (200 mosmolal) evoked the activation of both 36Cl- influx and efflux, which were insensitive to inhibitors of the anion exchanger and of the anion/cation cotransport, and conversely were inhibited by the Cl(-)-channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). 36Cl- efflux was linked to a parallel efflux of 86Rb+; thus conductive K+ and Cl- pathways are activated during volume regulation in human fibroblasts. This conclusion is supported by evidence that, in hypotonic medium, 36Cl- influx and 86Rb+ efflux were both enhanced by depolarization of the plasma membrane. Depletion of the intracellular K+ content, obtained by preincubation with the ionophore gramicidin in Na(+)-free medium, had no effect on Cl- efflux in hypotonic medium. This result has been interpreted as evidence for independent activation of K+ and Cl- pathways. It is also concluded that the anion permeability is the rate-limiting factor in the response of human fibroblasts to hypotonic stress.
authors.affiliation: Dipartimento di Biologia Ev. Sp., Università di Bologna, Italia.
authors.forename: T
authors.initials: T
authors.lastname: Mastrocola
authors.forename: A
authors.initials: A
authors.lastname: Flamigni
authors.forename: M
authors.initials: M
authors.lastname: Rugolo
mesh_terms: D001692:Biological Transport / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism*; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D006096:Gramicidin / Q000494:pharmacology; D006801:Humans; D007038:Hypotonic Solutions; D009994:Osmolar Concentration; D009997:Osmotic Pressure; D011188:Potassium / Q000378:metabolism*; D012414:Rubidium Radioisotopes / Q000378:metabolism
chemical_list: D002712:Chlorides; D007038:Hypotonic Solutions; D012414:Rubidium Radioisotopes; D006096:Gramicidin; D011188:Potassium