Upper airway neurogenic mechanisms.

Abstract

Stimulation of the nasal sensory nerves leads to sensations of pain and stuffiness. Type C nociceptive nerve releases neuropeptides including substance P and calcitonin gene related peptides that increase plasma extravasation and glandular secretion. This axonal response acts as an immediate protective mucosal defense mechanism. Recruited parasympathetic reflexes cause submucosal gland secretion via acetylcholine and muscarinic M(3) receptors. Itching, sneezing, and other avoidance behaviors rapidly clear the offending agents from the upper airways and protect the lower airways. Dysfunction of these nerves may contribute to allergic rhinitis, infectious rhinitis, nasal hyperresponsiveness, and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, and so restores nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies. Human axon responses differ from those in animals, an important distinction that limits extrapolation from other species.