Cardiac transient outward potassium current

The cardiac transient outward potassium current (referred to as I_to1 or I_to

I_to1 is rapidly activated and deactivated.[2] It is activated after the fast increase of the membrane potential following the phase 0 of the cardiac action potential. Once activated, (K⁺) ions from inside the cells flow to the extracellular space. This outward flow of positively charged ions constitutes the I_to1 and causes the transmembrane voltage to decrease. This decrease of the transmembrane potential is known as repolarization. I_to1 is then quickly deactivated, stopping the repolarization and ending the phase 1 of the action potential.

I_to1 is

I_to1 affects the opening of Ca²⁺ channels during Phase 2 of the Action Potential. As a result, changes in I_to1 modulate changes in the action potential duration.[2]

Role in disease

• Reduction in I_to1 density is associated with prolonged action potentials and is a common finding in
  cardiac disease .^[3]

• I_to1 density is significantly lower in the cells of a failing heart in comparison to the cells of a healthy heart.^[4]
• There is correlation between decreased I_to1 density and atrial fibrillation.^[5]
• I_to activation is inhibited by
  thyrotropin (TSH).^[6] This mechanisms may be one of the reasons for the observation that both bradycardia and atrial fibrillation are common in hypothyroidism.^[7][8][9]

• An increase in the I_to1 density caused by a mutation in Kv4.3 can be a cause of
  Brugada Syndrome.^[10]