Although the mechanisms of asthma, a disease that affects 6 million Americans, are unclear, recent observations demonstrating the major role played by immunologic mechanisms and inflammatory cells and their products in the pathogenesis and perpetuation of asthma represent major A developments in the field of allergy.
Airway diameter appears to be regulated in part by the autonomic nervous system through a carefully controlled balance between cholinergic and α-adrenergic bronchoconstrictor and β2-adrenergic bronchodilator effects. Bronchial smooth-muscle tone and mast cell—mediator release are known to be regulated in part by neurochemical stimulation of these cell receptors. Thus, the finding that autonomic receptor abnormalities, including increased sensitivity to α-adrenergic and cholinergic stimuli and insensitivity to β2-agonists, are common in patients with allergic diseases in general, and asthma in particular, is of special interest.1 In this regard, it has recently been shown that a subset of as much as 5% of
deShazo RD, Salvaggio JE. Allergy and Immunology. JAMA. 1985;254(16):2257–2259. doi:10.1001/jama.1985.03360160089017
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