Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sympathetic and parasympathetic influences on the airway resistance under physiological and pathophysiological conditions have long been known. In recent years, this classical view had to be extended due to mounting evidence of neurocrine and paracrine peptide mediators. The term non-adrenergic non-cholinergic (NANC) nervous system was coined. Besides other effects the non-adrenergic mediators (e.g. VIP and PHI/PHM) give rise to bronchodilation, while the non-cholinergic modulators (SP, neurokinin A, and CGRP) induce bronchospasm. The axon-reflex theory postulates liberation of non-cholinergic peptide substances by afferent C-fibers exposed by bronchial epithelial cell damage as one important cause of bronchial obstruction. In addition to biogenic amines, such peptides as bombesin, leu-encephalin, beta-endorphin, calcitonin, doctrine cells of the bronchial epithelium. Our knowledge of the biological relevance of these mediators is at present very sketchy. Platelet activating factor (PAF) is released by alveolar macrophages, granulocytes, blood vessel endothelium, and platelets. The inhalation of PAF induces bronchospasm in healthy subjects and asthmatics and also prolonged bronchial hyperreactivity. The many factors influencing bronchial reactivity need to be classified by further investigations of the mode of interaction and interdependence of known and new mediators.
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PMID:[The significance of endocrine, neurocrine and paracrine mediators in the regulation of bronchial reactivity]. 268 1