title: Volume regulation in NIH/3T3 cells not expressing P-glycoprotein. I. Regulatory volume decrease.
abstract: Exposure of NIH/3T3 fibroblasts not expressing P-glycoprotein to 50, 30, 20, and 10% hyposmotic solutions led to cell volume increases of 70, 32, 21, and 12%, respectively. After swelling, NIH/3T3 cells exhibited regulatory volume decrease (RVD), attaining complete volume recovery after 30 min except in 50% hyposmotic solution, in which volume recovery was 76%. RVD was accelerated by gramicidin and inhibited by the Cl channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoic acid, 1,9-dideoxyforskolin, dipyridamole, and niflumic acid and by the K channel, blocker quinidine. RVD was reduced 15% by removal of extracellular Ca. The pathway opened by hypotonicity was highly permeable to K and Rb and only partly permeable to other cations. Most anions were able to permeate, with a permeability ranking of nitrate > benzoate = iodide > thiocyanate > chloride > > gluconate. The pathway was permeable to neutral amino acids, with a permeability ranking of glycine > alanine > glutamate > taurine > gamma-aminobutyric acid > glutamine. The pathway was not permeable to basic amino acids. These results show that, despite the absence of P-glycoprotein, NIH/3T3 cells exhibit RVD with properties similar to those expressed in most cell types.
authors.affiliation: Institute of Cell Physiology, National University of Mexico, Mexico City, Mexico.
authors.forename: H
authors.initials: H
authors.lastname: Pasantes-Morales
authors.forename: R
authors.initials: R
authors.lastname: Sánchez Olea
authors.forename: D
authors.initials: D
authors.lastname: Miranda
authors.forename: J
authors.initials: J
authors.lastname: Morán
mesh_terms: D016475:3T3 Cells; D015761:4-Aminopyridine / Q000494:pharmacology; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000032:analysis / Q000502:physiology*; D000818:Animals; D000838:Anions / Q000378:metabolism*; D001464:Barium / Q000494:pharmacology; D002463:Cell Membrane Permeability; D018118:Chloride Channels / Q000037:antagonists & inhibitors / Q000502:physiology*; D002712:Chlorides / Q000378:metabolism* / Q000494:pharmacology; D003078:Colchicine / Q000633:toxicity; D005576:Colforsin / Q000031:analogs & derivatives / Q000494:pharmacology; D004176:Dipyridamole / Q000494:pharmacology; D006096:Gramicidin / Q000494:pharmacology; D007700:Kinetics; D051379:Mice; D009544:Niflumic Acid / Q000494:pharmacology; D009579:Nitrobenzoates / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology; D011802:Quinidine / Q000494:pharmacology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology*
chemical_list: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D000838:Anions; D018118:Chloride Channels; D002712:Chlorides; D009579:Nitrobenzoates; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D006096:Gramicidin; D005576:Colforsin; D001464:Barium; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D009544:Niflumic Acid; D004176:Dipyridamole; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D011802:Quinidine; C047983:1,9-dideoxyforskolin; D003078:Colchicine