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Updated: May 31, 2026
04:33
Methods for Detecting Cough and Airway Inflammation in Mice
Published on: August 2, 2024
G-protein coupled receptors regulating cough
Sarah A Maher1, Eric D Dubuis, Maria G Belvisi
1Respiratory Pharmacology, Pharmacology & Toxicology Section, Imperial College London, Faculty of Medicine, National Heart and Lung Institute, Sir Alexander Fleming Building, London SW7 2AZ, UK.
Current Opinion in Pharmacology
|July 6, 2011
Summary
Coughing can be controlled by G protein-coupled receptors (GPCRs). Research suggests beta2-adrenoceptor activation inhibits cough by hyperpolarizing nerves, challenging previous models.
Area of Science:
- Pharmacology
- Neuroscience
- Respiratory Medicine
Background:
- Cough is a vital reflex but can become pathological.
- G protein-coupled receptors (GPCRs) modulate cough reflex pathways.
- Airway sensory nerves are activated by mediators like prostaglandin E2 and bradykinin via EP3, B2, TRPV1, and TRPA1 receptors.
Purpose of the Study:
- To investigate the inhibitory mechanisms of cough suppression.
- To elucidate the signaling pathway of beta2-adrenoceptor mediated cough inhibition.
- To explore the role of cyclic GMP and BKCa channels in cough reflex modulation.
Main Methods:
- Review of current literature on cough reflex pathways.
- Analysis of signaling cascades involved in sensory nerve modulation.
- Examination of receptor-ligand interactions in the airways.
Main Results:
- Beta2-adrenoceptor and cannabinoid CB2 receptors inhibit cough by suppressing sensory nerve activity.
- The canonical pathway for beta2-adrenoceptor activation involves cAMP-PKA.
- Emerging evidence points to a PKG-mediated pathway involving BKCa channel opening and nerve hyperpolarization.
Conclusions:
- The understanding of beta2-adrenoceptor signaling in cough suppression is evolving.
- PKG-mediated BKCa channel activation represents a novel mechanism for cough inhibition.
- Targeting these pathways may offer new therapeutic strategies for cough disorders.
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