title: Evidence for voltage-sensitive, calcium-conducting channels in airway epithelial cells.
abstract: In airways epithelial cultures, mechanical stimulation induces intracellular Ca2+ concentration ([Ca2+]i) changes by causing Ca2+ entry and intracellular Ca2+ release. Mechanically induced Ca2+ fluxes across the plasma membrane are blocked by Ni2+ (Boitano, S., M. J. Sanderson, and E. R. Dirksen. J. Cell. Sci. 107: 3037-3044, 1994). In this report we use fluorescence imaging microscopy with fura 2 and intracellular recording of the transmembrane potential to further characterize Ca2+ flux in the plasma membrane of these cells. Mechanically induced Ca2+ influx is blocked by nifedipine. Addition of the dihydropyridine agonist BAY K8644 (2 microM) leads to a delayed increase of [Ca2+]i that is dependent on extracellular Ca2+. Switching to high extracellular K+ concentration ([K+]o) causes depolarization of the plasma membrane and a transient increase in [Ca2+]i. The number of cells that respond to high [K+]o is significantly decreased by Ni2+ (1 mM) or nifedipine (10 microM). Mechanical stimulation causes a rapid depolarization of the stimulated cell that can be suppressed by the K+ ionophore valinomycin. Valinomycin treatment also blocks mechanically induced Ca2+ dux. These results suggest that voltage-sensitive Ca(2+)-conducting channels exist in airway epithelial cells, and these channels contribute to the [Ca2+]i changes observed after mechanical stimulation or depolarization of the plasma membrane.
authors.affiliation: Department of Neurobiology, University of California, Los Angeles, School of Medicine 90095-1763, USA.
authors.forename: S
authors.initials: S
authors.lastname: Boitano
authors.forename: M L
authors.initials: ML
authors.lastname: Woodruff
authors.forename: E R
authors.initials: ER
authors.lastname: Dirksen
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004594:Electrophysiology; D008564:Membrane Potentials / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D009994:Osmolar Concentration; D010812:Physical Stimulation; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D014132:Trachea / Q000166:cytology / Q000378:metabolism*; D014634:Valinomycin / Q000494:pharmacology
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D014634:Valinomycin; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D011188:Potassium; D002118:Calcium