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ANESTHETIC PHARMACOLOGY

Involvement of Adenosine Triphosphate-Sensitive Potassium Channels in the Response of Membrane Potential to Hyperosmolality in Cultured Human Aorta Endothelial Cells

Department of Anesthesiology, Tokushima University School of Medicine, Tokushima, Japan

Address correspondence and reprint requests to Dr. Yoshinobu Tomiyama, Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. Address e-mail to tomi{at}clin.med.tokushima-u.ac.jp.

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 H₂O) containing 200 nM bis-(1,3-diethylthiobarbiturate)trimethine oxonol and exposed to 315 and 345 mOsm/kg H₂O hyperosmotic medium sequentially in the presence and absence of 1 µM glibenclamide, a well-known K_ATP channel blocker. Hyperosmotic mannitol significantly induced hyperpolarization of the endothelial cells, which was prevented by 1 µM glibenclamide (n = 6). Estimated changes of membrane potential at 315 and 345 mOsm/kg H₂O 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 µM 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.