title: Volume-activated K+ and Cl- pathways of dissociated eccrine clear cells.
abstract: In isolated rhesus eccrine clear cells, regulatory volume decrease (RVD) occurs after osmotic swelling. RVD was completely inhibited by 1 mM quinidine, 200 nM charybdotoxin, 1 mM diphenylamine-2-carboxylic acid (DPC), or 0.1 mM 4-nitro-2(3-phenylpropyl-amino)benzoate. RVD was also inhibited in Ca(2+)-free medium by vinblastine (antimicrotubular agent), N-(6-aminohexyl)-5-chloro-1- naphthalenesulfonamide (W-7), or 0.1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Valinomycin reversed quinidine- and DIDS-induced inhibition of RVD but not the inhibition caused by Ca(2+)-free medium, DPC, vinblastine, or W-7. The cytosolic free Ca2+ concentration, as determined by the fura 2 method, increased from 220 nM in the control to 435 nM during RVD. Activation of both K+ and Cl-currents was also directly demonstrated with the whole cell current-voltage clamp method. DIDS inhibited swelling-induced K+, but not Cl-, currents and depolarized the membrane potential during RVD, further supporting the notion that DIDS inhibited swelling-activated K+, but not Cl-, pathways. We conclude that the observed RVD is mediated by the activation of conductive Ca(2+)-dependent K+ and Cl- pathways.
authors.affiliation: Marshall Dermatology Research Laboratories, Department of Dermatology, University of Iowa, College of Medicine, Iowa City 52242.
authors.forename: G
authors.initials: G
authors.lastname: Samman
authors.forename: M
authors.initials: M
authors.lastname: Ohtsuyama
authors.forename: F
authors.initials: F
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Sato
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000818:Animals; D001706:Biopsy; D002118:Calcium / Q000494:pharmacology; D002147:Calmodulin / Q000037:antagonists & inhibitors; D002478:Cells, Cultured; D018999:Charybdotoxin; D002712:Chlorides / Q000378:metabolism*; D004439:Eccrine Glands / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004533:Egtazic Acid / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects; D007038:Hypotonic Solutions; D008253:Macaca mulatta; D008564:Membrane Potentials / Q000187:drug effects; D009579:Nitrobenzoates / Q000494:pharmacology; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*; D012604:Scorpion Venoms / Q000494:pharmacology; D012867:Skin / Q000166:cytology; D013449:Sulfonamides / Q000494:pharmacology; D014634:Valinomycin / Q000494:pharmacology; D014747:Vinblastine / Q000494:pharmacology; D062367:ortho-Aminobenzoates / Q000494:pharmacology
chemical_list: D002147:Calmodulin; D002712:Chlorides; D007038:Hypotonic Solutions; D009579:Nitrobenzoates; D012604:Scorpion Venoms; D013449:Sulfonamides; D062367:ortho-Aminobenzoates; D018999:Charybdotoxin; D014634:Valinomycin; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D004533:Egtazic Acid; D014747:Vinblastine; C017967:W 7; C001209:fenamic acid; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D011188:Potassium; D002118:Calcium