Cardiac fibroblasts and the mechano-electric feedback mechanism in healthy and diseased hearts

Prog Biophys Mol Biol. May-Jul 2003;82(1-3):111-20. doi: 10.1016/s0079-6107(03)00009-9.

Abstract

Cardiac arrhythmia is a serious clinical condition, which is frequently associated with abnormalities of mechanical loading and changes in wall tension of the heart. Recent novel findings suggest that fibroblasts may function as mechano-electric transducers in healthy and diseased hearts. Cardiac fibroblasts are electrically non-excitable cells that respond to spontaneous contractions of the myocardium with rhythmical changes of their resting membrane potential. This phenomenon is referred to as mechanically induced potential (MIP) and has been implicated in the mechano-electric feedback mechanism of the heart. Mechano-electric feedback is thought to adjust the frequency of spontaneous myocardial contractions to changes in wall tension, which may result from variable filling pressure. Electrophysiological recordings of single atrial fibroblasts indicate that mechanical compression of the cells may activate a non-selective cation conductance leading to depolarisation of the membrane potential. Reduced amplitudes of MIPs due to pharmacological disruption of F-actin and tubulin suggest a role for the cytoskeleton in the mechano-electric signal transduction process. Enhanced sensitivity of the membrane potential of the fibroblasts to mechanical stretch after myocardial infarction correlates with depression of heart rates. It is assumed that altered electrical function of cardiac fibroblasts may contribute to the increased risk of post-infarct arrhythmia.

Publication types

  • Review

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / metabolism
  • Cells, Cultured
  • Cytoskeleton / metabolism
  • Electrophysiology
  • Fibroblasts / metabolism*
  • Gadolinium / pharmacology
  • Gap Junctions
  • Heart Atria / metabolism
  • Humans
  • Ions / metabolism
  • Membrane Potentials
  • Models, Cardiovascular
  • Myocardial Contraction
  • Myocardial Infarction
  • Myocardium / cytology*
  • Myocardium / metabolism
  • Rats
  • Signal Transduction
  • Stress, Mechanical

Substances

  • Ions
  • Gadolinium