Cardiac Na Channels: Structure to Function

Curr Top Membr. 2016:78:287-311. doi: 10.1016/bs.ctm.2016.05.001. Epub 2016 Jun 14.

Abstract

Heart rhythms arise from electrical activity generated by precisely timed opening and closing of ion channels in individual cardiac myocytes. Opening of the primary cardiac voltage-gated sodium (NaV1.5) channel initiates cellular depolarization and the propagation of an electrical action potential that promotes coordinated contraction of the heart. The regularity of these contractile waves is critically important since it drives the primary function of the heart: to act as a pump that delivers blood to the brain and vital organs. When electrical activity goes awry during a cardiac arrhythmia, the pump does not function, the brain does not receive oxygenated blood, and death ensues. Perturbations to NaV1.5 may alter the structure, and hence the function, of the ion channel and are associated downstream with a wide variety of cardiac conduction pathologies, such as arrhythmias.

Keywords: Kinetic processes; Na channel; Na(V)1.5; SCN5A; Structure and function.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials
  • Allosteric Regulation
  • Animals
  • Channelopathies / metabolism
  • Channelopathies / pathology
  • Humans
  • Myocytes, Cardiac / metabolism*
  • NAV1.5 Voltage-Gated Sodium Channel / chemistry
  • NAV1.5 Voltage-Gated Sodium Channel / metabolism
  • Nuclear Magnetic Resonance, Biomolecular
  • Protein Processing, Post-Translational
  • Protein Structure, Quaternary
  • Protein Subunits / chemistry
  • Protein Subunits / metabolism
  • Voltage-Gated Sodium Channels / chemistry
  • Voltage-Gated Sodium Channels / metabolism*

Substances

  • NAV1.5 Voltage-Gated Sodium Channel
  • Protein Subunits
  • Voltage-Gated Sodium Channels