Involvement of adenosine triphosphate-sensitive potassium channels in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells.
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.
Yamaguchi
Mikiyo
M
Department of Anesthesiology, Tokushima University School of Medicine, Tokushima, Japan.
Tomiyama
Yoshinobu
Y
Katayama
Toshiko
T
Kitahata
Hiroshi
H
Oshita
Shuzo
S
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
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