Airway sensory innervation as a target for novel therapies: an outdated concept?
Sensory nerves in the airways regulate central and local reflex events such as bronchoconstriction, airway plasma leakage, mucus secretion and cough. Sensory nerve activity can be enhanced during inflammation and, as a result, these protective reflexes become exacerbated and deleterious. The development of drugs that directly inhibit sensory nerve function has again become an attractive target for the pharmaceutical industry. In particular, the focus is on inhibition of the symptoms associated with airway inflammatory diseases such as asthma, chronic obstructive pulmonary disease and cough of any aetiology.
Belvisi
Maria G
MG
Respiratory Pharmacology Group, Cardiothoracic Surgery, National Heart and Lung Institute, Faculty of Medicine, Imperial College, Dovehouse Street, London SW3 6LY, UK. m.belvisi@ic.ac.uk
D016084:Bronchoconstriction / Q000187:drug effects; D016503:Drug Delivery Systems; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D009093:Mucus / Q000378:metabolism; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology; D011661:Pulmonary Stretch Receptors / Q000187:drug effects / Q000503:physiopathology; D012137:Respiratory System / Q000187:drug effects* / Q000294:innervation* / Q000503:physiopathology; D019141:Respiratory System Agents / Q000494:pharmacology*; D011984:Sensory Receptor Cells / Q000187:drug effects* / Q000503:physiopathology
D019141:Respiratory System Agents