Nasal pathophysiology.

The major pathological changes in rhinitis are vascular, with blood sinus congestion, transudation and oedema, and glandular, with mucus secretion. Both block the nose. Mediators released by antigen-antibody reactions and by inflammatory processes will disrupt nasal function in three main ways. First, mediators such as histamine, bradykinin and leukotrienes will act directly on blood vessels and submucosal glands, causing mucosal thickening and secretion. Second, the same mediators will excite terminals of sensory nervous receptors in the nose, setting up axon reflexes with release of neuropeptides from other branches of the nervous receptors. Neurokinins, such as substance P, will augment vasodilatation and transudation and may modulate the secretions from submucosal glands. Third, the same sensory receptors when stimulated will set up central nervous reflex actions. The responses include sneezing and nasal irritation (both prominent features of rhinitis) reflex nasal vasodilatation and mucus secretion, and actions on the lower airways. The relative importance of these three mechanisms is difficult to assess in man. Successful therapy may act by preventing one of the undesirable motor constituents of rhinitis, or may have a more general action in lessening inflammation or immunological responses.