Regulation of Mucus Secretion in Airways
Abstract:Delayed mucociliary clearance occurs in asthmatic subjects, and postmortem studies demonstrate gland hypertrophy and inspissated secretions plugging the airways in these patients. Abnormalities in secret ion of fluid and mucus are likely to be involved in the pathogenesis of these disorders. This chapter covers gland regulation. Most of the mucus in airways is normal produced by the glands, which are under both neural and humoral regulation. Cholinergic, adrenergic and non-cholinergic neural modulation have been demonstrated. Vagal reflexes increase gland output markedly. Mechanical, chemical, and pharmacologic stimuli are the most potent initiators of vagal reflex secretion. Inflammatory diseases may produce excessive secretion by reflex irritation of the airway mucosa. Glands contain serous and mucous cells; selective stimulation of serous cells by alpha-adrenergic agonists or of mucous cells by beta-adrenergic agonists, markedly alters the viscoelastic properties of secretions produced. Imbalance between these two adrenergic systems in disease could affect the secretions adversely. Modification of the viscoelastic properties of the secretions by selective drug therapy may improve clearance. Various drugs and mediators have profound effects on submucosal gland secretion. Preformed mediators, such as histamine, are mild secretogogues. Metabolites of arachidonate metabolism, including prostaglandins and leukotrienes, are potent secretogogues. These metabolites are secreted by many of the cells that normally reside in the a (e.g., epithelial cells, muscle cells, fibroblasts, mast cells) and by cells that normally reside in the bloodstream and move to the airways during inflammation (e.g., neutrophils). There is presently a great deal of evidence implicating inflammatory "cascades" in the pathogenesis of asthma (both "intrinsic" and "extrinsic"). Inflammation of the airway epithelium, by stimulating both neural and humoral pathways, probably plays a predominant role in the development of status asthmaticus. Drugs, such as steroids, probably improve the patient's status by salutory is effects on these inflammatory processes. Future therapy is likely to be directed to inhibition of specific pathways activated by these inflammatory cascades.
Document Type: Research Article
Affiliations: Physiology and Radiology, University of California, San Francisco, San Francisco, CA 94143
Publication date: 1984-06-01
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