Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1996:58:363-94.
doi: 10.1146/annurev.ph.58.030196.002051.

Myocardial potassium channels: electrophysiological and molecular diversity

Affiliations
Review

Myocardial potassium channels: electrophysiological and molecular diversity

D M Barry et al. Annu Rev Physiol. 1996.

Abstract

Myocardial K+ currents function to control resting membrane potentials, the heights and durations of action potentials, and refractoriness and automaticity. They are important targets for the actions of transmitters and hormones or drugs known, or postulated, to modulate cardiac functioning. A variety of K+ currents that subserve these functions have now been identified in myocardial cells isolated from different species, as well as in cells isolated from different regions of the heart in the same species. These currents include the voltage-gated K+ types, such as the transient outward (Ito) and delayed rectifier (IK) currents, as well as the inwardly rectifying currents, IK1, IK(ACh), and IK(ATP). The physiological and functional properties of the various K+ currents/channels expressed in different myocardial cell types are the focus of this review. Advances made in cloning K+ channel subunits of the Kv, eag, Kir, and IsK families are discussed, and progress made in identifying the K+ channel subunits expressed in the mammalian myocardium is summarized. The relationships between the various cloned K+ channel subunits and the functional K+ channels characterized electrophysiologically in myocardial cells are explored.

PubMed Disclaimer

Publication types

Substances

LinkOut - more resources