What is it about?

Noradrenaline (NA), the neurotransmitter responsible for increasing the rate and strength of the heartbeat during exercise, is also involved in triggering atrial fibrillation, an abnormal heart rhythm. The mechanisms of NA action in the atria remain unclear. In this study, we showed that, in rat single atrial cells, NA slows the recovery of the electrical impulse by inhibiting a pore for potassium ions to cross the cell membrane. This involved two forms of beta-receptor for NA working together.

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Why is it important?

This study provides good evidence of a role for a TREK-like potassium channel in repolarisation of rat atrial myocytes and a role for that channel in mediating the effects of noradrenaline on atrial electrophysiology. Evidence for a cooperative action of beta-1 and beta-2 adrenoceptors in the effect of NA is provided. If this mechanism is shown to exist in the human atrium, both the channels and receptors may have potential as therapeutic targets in atrial fibrillation. Further work is merited.

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This page is a summary of: Inhibition of a TREK-like K+ channel current by noradrenaline requires both β1- and β2-adrenoceptors in rat atrial myocytes, Cardiovascular Research, October 2014, European Society of Cardiology,
DOI: 10.1093/cvr/cvu192.
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