Abstract
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.
- ,
- 12509475
- action
- adenoviridae,
- animals,
- calcium,
- cardiac,
- cardiovascular,
- cell
- channels,
- contraction,
- electric
- electrophysiology,
- gov't,
- heart
- heterozygote,
- humans,
- immunoblotting,
- inwardly
- line,
- membrane
- models,
- mutagenesis,
- mutation,
- myocardial
- myocardium,
- myocytes,
- non-u.s.
- patch-clamp
- pota,
- potassium
- potentials,
- rabbits,
- rectifying,
- research
- reticulum,
- sarcoplasmic
- site-directed,
- ssium
- stimulation,
- support,
- techniques,
- ventricles,
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