Airway epithelium-derived relaxing factor: myth, reality, or naivety?

Am J Physiol Cell Physiol. 2013 May 1;304(9):C813-20. doi: 10.1152/ajpcell.00013.2013. Epub 2013 Jan 16.

Abstract

The presence of a healthy epithelium can moderate the contraction of the underlying airway smooth muscle. This is, in part, because epithelial cells generate inhibitory messages, whether diffusible substances, electrophysiological signals, or both. The epithelium-dependent inhibitory effect can be tonic (basal), synergistic, or evoked. Rather than a unique epithelium-derived relaxing factor (EpDRF), several known endogenous bronchoactive mediators, including nitric oxide and prostaglandin E2, contribute. The early concept that EpDRF diffuses all the way through the subepithelial layers to directly relax the airway smooth muscle appears unlikely. It is more plausible that the epithelial cells release true messenger molecules, which alter the production of endogenous substances (nitric oxide and/or metabolites of arachidonic acid) by the subepithelial layers. These substances then diffuse to the airway smooth muscle cells, conveying epithelium dependency.

Keywords: bronchi; nitric oxide; prostaglandin E2; relaxing factors; trachea.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bronchioles / cytology
  • Bronchioles / physiology
  • Humans
  • Intercellular Signaling Peptides and Proteins / physiology
  • Muscle, Smooth, Vascular / physiology
  • Paracrine Communication*
  • Respiratory Mucosa / physiology*
  • Signal Transduction

Substances

  • Intercellular Signaling Peptides and Proteins