title: Involvement of adenosine triphosphate-sensitive potassium channels in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells.
abstract: The membrane potential of endothelial cells is an important determinant of endothelial functions, including regulation of vascular tone. We investigated whether adenosine triphosphate-sensitive potassium (K(ATP)) channels were involved in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells. The voltage-sensitive fluorescent dye, bis-(1,3-diethylthiobarbiturate)trimethine oxonol, was used to assess relative changes in membrane potential semiquantitatively. To investigate the effect of mannitol-, sucrose-, and NaCl-induced hyperosmolality on membrane potential, cells were continuously perfused with Earle's balanced salt solution (285 mOsm/kg H(2)O) containing 200 nM bis-(1,3-diethylthiobarbiturate)trimethine oxonol and exposed to 315 and 345 mOsm/kg H(2)O hyperosmotic medium sequentially in the presence and absence of 1 muM glibenclamide, a well-known K(ATP) channel blocker. Hyperosmotic mannitol significantly induced hyperpolarization of the endothelial cells, which was prevented by 1 microM glibenclamide (n = 6). Estimated changes of membrane potential at 315 and 345 mOsm/kg H(2)O were 13 +/- 8 and 21 +/- 8 mV, respectively. Hypertonic sucrose induced similar changes. However, although hypertonic saline also significantly induced hyperpolarization of the endothelial cells (n = 6), the hyperpolarization was not prevented by 1 muM glibenclamide. In conclusion, K(ATP) channels may participate in hyperosmotic mannitol- and sucrose-induced hyperpolarization, but not in hypertonic saline-induced hyperpolarization in cultured human aorta endothelial cells.
authors.affiliation: Department of Anesthesiology, Tokushima University School of Medicine, Tokushima, Japan.
authors.forename: Mikiyo
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Tomiyama
authors.forename: Toshiko
authors.initials: T
authors.lastname: Katayama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kitahata
authors.forename: Shuzo
authors.initials: S
authors.lastname: Oshita
mesh_terms: D018528:ATP-Binding Cassette Transporters; D001011:Aorta / Q000166:cytology / Q000187:drug effects; D002138:Calibration; D002478:Cells, Cultured; D019806:Cromakalim / Q000494:pharmacology; D004234:Diuretics, Osmotic / Q000494:pharmacology; D042783:Endothelial Cells / Q000502:physiology*; D005456:Fluorescent Dyes; D005905:Glyburide / Q000494:pharmacology; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007202:Indicators and Reagents; D054086:KATP Channels; D008353:Mannitol / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009994:Osmolar Concentration; D010477:Perfusion; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying; D012965:Sodium Chloride / Q000494:pharmacology; D013395:Sucrose / Q000494:pharmacology; D013858:Thiobarbiturates; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018528:ATP-Binding Cassette Transporters; D004234:Diuretics, Osmotic; D005456:Fluorescent Dyes; D007004:Hypoglycemic Agents; D007202:Indicators and Reagents; D054086:KATP Channels; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D013858:Thiobarbiturates; D014665:Vasodilator Agents; C092520:uK-ATP-1 potassium channel; D019806:Cromakalim; D008353:Mannitol; D012965:Sodium Chloride; C025284:bis(1,3-diethylthiobarbiturate)trimethineoxonol; D013395:Sucrose; D005905:Glyburide