The transient outward potassium current (Ito) modulates cardiac excitation-contraction coupling through its influence on L-type Ca2+ channels and is invariably reduced in heart disease.
The cardiac action potential (AP) is critical for initiating and coordinating myocyte contraction. In particular, the early repolarization period of the AP (phase 1) strongly influences the time course and magnitude of the whole-cell intracellular Ca(2+) transient by modulating trans-sarcolemmal Ca(2+) influx through L-type Ca(2+) channels (I(Ca,L)) and Na-Ca exchangers (I(Ca,NCX)). The transient outward potassium current (I(to)) has kinetic properties that make it especially effective in modulating the trajectory of phase 1 repolarization and thereby cardiac excitation-contraction coupling (ECC). The magnitude of I(to) varies greatly during cardiac development, between different regions of the heart, and is invariably reduced as a result of heart disease, leading to corresponding variations in ECC. In this article, we review evidence supporting a modulatory role of I(to) in ECC through its influence on I(Ca,L), and possibly I(Ca,NCX). We also discuss differential effects of I(to) on ECC between different species, between different regions of the heart and in heart disease.
Sah et al. (Wed,) conducted a review in Heart disease. Transient outward potassium current (Ito) was evaluated. The transient outward potassium current (Ito) modulates cardiac excitation-contraction coupling through its influence on L-type Ca2+ channels and is invariably reduced in heart disease.