Mediators and reflex bronchoconstriction.
Reflex bronchoconstriction can be induced by mechanical and chemical stimuli to the respiratory tract, especially from the larynx down to the larger intrapulmonary airways. The pathways for these reflexes have been analysed in experimental animals. The afferent nerves include fibres from rapidly adapting ("irritant") receptors in and under the epithelium of the airways, and those from "C-fibre" receptors in the tracheobronchial tree and possible alveoli. Many of the mediators thought to be released in lung antigen antibody reactions and airway tissue damage can be shown to activate these groups of sensory receptors: the mediators include prostaglandins, bradykinin, histamine and 5-hydroxytryptamine. Both the irritant and the C-fibre receptors have been shown to cause reflex bronchoconstriction, as well as other reflex motor actions that influence the diameter of the respiratory tract, such as mucus secretion and laryngeal constriction. They are also responsible for respiratory changes, including coughing. Mediators which are released in bronchial asthma are potential agents in setting up reflex bronchoconstriction. In man the evidence for such a reflex depends primarily on the inhibitory efficiency of atropinic drugs in some forms of asthma. Such evidence cannot be completely unequivocal but, taken with the analogy with animal experiments, there seems to be a prima facie case for reflex bronchoconstriction as one component of the total pattern of an asthma attack.
D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000294:innervation / Q000503:physiopathology*; D006801:Humans; D009305:Nasopharynx / Q000503:physiopathology; D009412:Nerve Fibers / Q000502:physiology; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D012018:Reflex