Journal
CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY
Volume 2, Issue 1, Pages 11-19Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00130832-200202000-00003
Keywords
-
Categories
Funding
- Kaohsiung Medical University, Taiwan
- US Public Health Service Award [RO1 A142403]
- Department of Defense [170020018]
- Environmental Protection Agency [R825814]
- United States Environmental Protection Agency [R825814]
Ask authors/readers for more resources
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 muco blood flow, sinusoidal filling, and mucosal thickness, and restores nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies. Hu axon responses differ from those in animals, an important distinction that limits extrapolation from other species. (C) 2002 Lippincott Williams & Wilkins.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available