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Cardiac transient outward potassium current

The cardiac transient outward potassium current (referred to as I<sub>to1</sub> or I<sub>to</sub>) is one of the ion currents across the cell membrane of heart muscle cells. It is responsible for the (brief) repolarizing phase 1 of the cardiac action potential (which succeeds depolarisation, and precedes the plateau phase). The I<sub>to</sub> is produced by movement of positively charged potassium (K<sup>+</sup>) ions from the intracellular into the extracellular space. It exhibits rapid activation and inactivation. I<sub>to1</sub> is complemented with I<sub>to2</sub> resulting from Cl<sup>−</sup> ions to form the transient outward current I<sub>to</sub>.

The I<sub>to1</sub> is generated by voltage-gated K+ channels Kv1.4, Kv4.2, and (especially) Kv4.3; these channels undergo ball-and-chain inactivation to terminate the current.

It occurs in atrial, ventricular, and conduction system cells. In ventricular myocardium, it is more potent in the epicardium than the endocardium; this transmural I<sub>to1</sub> gradient underlies the J wave ECG finding.

Role in disease

  • Reduction in I<sub>to1</sub> density is associated with prolonged action potentials and is a common finding in cardiac disease.
*I<sub>to1</sub> density is significantly lower in the cells of a failing heart in comparison to the cells of a healthy heart.
*There is correlation between decreased I<sub>to1</sub> density and atrial fibrillation.
*I<sub>to</sub> activation is inhibited by thyrotropin (TSH). This mechanisms may be one of the reasons for the observation that both bradycardia and atrial fibrillation are common in hypothyroidism.
  • An increase in the I<sub>to1</sub> density caused by a mutation in Kv4.3 can be a cause of Brugada Syndrome.

References