Cardiac transient outward potassium current
Ion current
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The cardiac transient outward potassium current (referred to as Ito1 or Ito[1]) 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).[2] The Ito is produced by movement of positively charged potassium (K+) ions from the intracellular into the extracellular space. It exhibits rapid activation and inactivation.[3] Ito1 is complemented with Ito2 resulting from Cl− ions to form the transient outward current Ito.[citation needed]
The Ito1 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.[3]
It occurs in atrial, ventricular, and conduction system cells. In ventricular myocardium, it is more potent in the epicardium than the endocardium; this transmural Ito1 gradient underlies the J wave ECG finding.[3]
Role in disease
- Reduction in Ito1 density is associated with prolonged action potentials and is a common finding in cardiac disease.[4]
- Ito1 density is significantly lower in the cells of a failing heart in comparison to the cells of a healthy heart.[5]
- There is correlation between decreased Ito1 density and atrial fibrillation.[6]
- Ito activation is inhibited by thyrotropin (TSH).[7] This mechanisms may be one of the reasons for the observation that both bradycardia and atrial fibrillation are common in hypothyroidism.[8][9][10]
- An increase in the Ito1 density caused by a mutation in Kv4.3 can be a cause of Brugada Syndrome.[11]