Abstract
Adrenergic enhancement of the slowly activating delayed rectifier current (IKs) in cardiac myocytes constitutes a critical “repolarization reserve”. Stable co-expression of human (h)KCNQ1 and hKCNE1 in HEK-293 cells reconstitutes a native-like IKs current (HEK-IKs), allowing ß-adrenergic modulation of the current by stimulation of endogenous signalling pathways in the host cell line. HEK-IKs currents were enhanced two- to fourfold by bath application of isoproterenol (EC50 =13 nM), forskolin (10 μM), or 8-(4-chlorophenylthio) adenosine 3′,5′-cyclic monophosphate (50 μM), indicating an intact cAMP dependent ion channel-regulating pathway analogous to that observed in native cardiac myocytes.
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