Abstract
In the atria, the rapid delayed rectifier channels (IKr) are critical contributors to repolarization. In lipotoxic atria, increased functional expression of the serine/threonine mammalian target of rapamycin (mTOR) may remodel IKr and predispose to supraventricular arrhythmias. To investigate whether modulation of mTOR expression by palmitic acid exerts defects in the translational efficiency and gating mechanisms of IKr channel subunits hERG 1a/1b. Electrophysiology and biochemical assays in HEK293 cells and adult guinea pig atrial myocytes were used to assess the role of mTOR on protein expression and gating.
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