G-protein coupled receptors regulating cough

Curr Opin Pharmacol. 2011 Jun;11(3):248-53. doi: 10.1016/j.coph.2011.06.005. Epub 2011 Jul 2.

Abstract

Cough is a protective mechanism but can occur excessively in disease. Cough can be modulated by a range of GPCRs which can be either inhibitory or excitatory. Prostaglandin E2 and bradykinin can activate airway sensory nerves via EP3 and B2 receptors receptively and have both been shown to mediate their effects though TRPV1 and TRPA1 receptors. Activation of the β2-adrenoceptor and cannabinoid CB2 receptors can inhibit sensory nerves and prevent cough. It is currently thought that activation of the β2-adrenoceptor causes c-AMP dependent activation of PKA; however, recent research has suggested that the pathway involves PKG-mediated opening of the BKCa channel leading to hyperpolarization.

Publication types

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

MeSH terms

  • Animals
  • Cough / metabolism*
  • Humans
  • Receptors, G-Protein-Coupled / metabolism*
  • Sensory Receptor Cells / metabolism*
  • Signal Transduction

Substances

  • Receptors, G-Protein-Coupled