title: Calcium entry stimulated by swelling of Madin-Darby canine kidney cells.
abstract: Cell swelling in Madin-Darby canine kidney (MDCK) cells by reduction of extracellular osmolarity (omission of 70 ad 150 mmol/l mannitol, respectively) leads to the activation of anion of channels and Ca2+ sensitive K+ channels. The K+ channel activation leads to an initial transient hyperpolarization of the cell membrane potential (PD) followed by a sustained depolarization due to activation of anion channels. The present study elucidates the role of intracellular calcium (Ca2+i) in regulatory cell volume decrease (RVD) of MDCK cells. While reduction of extracellular osmolarity by omitting 70 mmol/l mannitol did not lead to a detectable change in Ca2+i, severe cell swelling by omitting 150 mmol/l mannitol led to a transient rise in Ca2+i. PD changes, on the other hand, were not different under either condition. In addition, the response of PD to cell swelling was not altered by treatment of the cells with 12-O-tetradecanoylphorbol-13-acetate diester, pertussis toxin or cholera toxin. In the nominal absence of extracellular Ca2+, reduction of extracellular osmolarity did not lead to an increase in Ca2+i and no initial transient hyperpolarization was observed, whereas addition of 10 mumol/l ATP still led to a significant hyperpolarization. Omission of extracellular Ca2+ was followed by a strong decrease in cell membrane resistance (Rm) due to activation of a depolarizing cation conductance. Subsequent readdition of Ca2+ caused a marked increase in Ca2+i due to Ca2+ influx. This Ca2+ entry was further stimulated by cell swelling. RVD was significantly blunted in the absence of extracellular Ca2+. The results suggest that cell swelling stimulates a Ca2+-permeable pathway in the cell membrane favoring Ca2+ entry into the cell with subsequent activation of Ca2+-sensitive K+ channels.
authors.affiliation: Hospital for Internal Medicine, University of Innsbruck, Austria.
authors.forename: E
authors.initials: E
authors.lastname: Wöll
authors.forename: M
authors.initials: M
authors.lastname: Ritter
authors.forename: T
authors.initials: T
authors.lastname: Haller
authors.forename: H
authors.initials: H
authors.lastname: Völkl
authors.forename: F
authors.initials: F
authors.lastname: Lang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002460:Cell Line / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D048429:Cell Size / Q000187:drug effects; D002772:Cholera Toxin / Q000494:pharmacology; D004285:Dogs; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000502:physiology; D007686:Kidney Tubules, Distal / Q000166:cytology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009994:Osmolar Concentration; D009995:Osmosis; D037342:Pertussis Toxin; D015221:Potassium Channels / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D010566:Virulence Factors, Bordetella; D002772:Cholera Toxin; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium