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(Circulation Research. 2001;89:336.)
© 2001 American Heart Association, Inc.

Cellular Biology

A TREK-1–Like Potassium Channel in Atrial Cells Inhibited by ß-Adrenergic Stimulation and Activated by Volatile Anesthetics

Cécile Terrenoire, Inger Lauritzen, Florian Lesage, Georges Romey, Michel Lazdunski

From the Institut de Pharmacologie Moléculaire et Cellulaire, Sophia Antipolis, Valbonne, France.

Correspondence to Prof Michel Lazdunski, Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UMR 6097, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France. E-mail ipmc{at}ipmc.cnrs.fr

Many members of the two-pore-domain potassium (K⁺) channel family have been detected in the mammalian heart but the endogenous correlates of these channels still have to be identified. We investigated whether I_KAA, a background K⁺ current activated by negative pressure (stretch) and by arachidonic acid (AA) and sensitive to intracellular acidification, could be the native correlate of TREK-1 in adult rat atrial cells. Using the inside-out configuration of the patch-clamp technique, we found that I_KAA, like TREK-1, was outwardly rectifying in physiological K⁺ conditions, with a conductance of 41 pS at +50 mV. Like TREK-1, I_KAA was reversibly activated by clinical concentrations of volatile anesthetics (in mmol/L, chloroform 0.18, halothane 0.11, and isoflurane 0.69). In cell-attached experiments, I_KAA was inhibited by chlorophenylthio-cAMP (500 µmol/L) and also by stimulation of ß-adrenergic receptors with isoproterenol (1 µmol/L). In addition, TREK-1 mRNAs were detected in all cardiac tissues, and the TREK-1 protein was immunolocalized in isolated atrial myocytes. Such a background potassium channel might contribute to the positive inotropic effects produced by ß-adrenergic stimulation of the heart. It might also be involved in the regulation of the atrial natriuretic peptide secretion.

Key Words: potassium channels • volatile anesthetics • ß-adrenergic receptor • heart cells

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