Neurogenic mechanisms in rhinosinusitis.
Nasal sensory nerve stimulation leads to sensations of pain and congestion and nociceptive nerve axon response-mediated release of substance P that stimulates glandular secretion as an immediate-acting protective mucosal defense. Recruited parasympathetic reflexes cause submucosal gland secretion via muscarinic M3 receptors. Parasympathetic reflexes, sneezing, and other avoidance behaviors rapidly clear the upper airway of offending agents while protecting the lower airways. Dysfunction contributes to allergic, infectious, and other nonallergic rhinitides and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, restoring nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies.
Baraniuk
J N
JN
Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, GL-020 Gorman Building, 3800 Reservoir Road, Washington, DC 20007-2197, USA. baraniuj@gunet.georgetown.edu
D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001369:Axons / Q000502:physiology; D006801:Humans; D009209:Myofascial Pain Syndromes / Q000150:complications / Q000503:physiopathology; D009297:Nasal Mucosa / Q000098:blood supply / Q000502:physiology; D020078:Neurogenic Inflammation / Q000150:complications* / Q000503:physiopathology*; D009475:Neurons, Afferent / Q000502:physiology; D012220:Rhinitis / Q000150:complications* / Q000503:physiopathology*; D012852:Sinusitis / Q000150:complications* / Q000503:physiopathology*