caa a22 4500 469049057 CHVBK 20180323132825.0 cr unu---uuuuu 170328e19920501xx s 000 0 eng 10.1007/BF00174316 doi (NATIONALLICENCE)springer-10.1007/BF00174316 Bai Tony Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, V6Z 1Y6, Vancouver, British Columbia, Canada aut Beta2 adrenergic receptors in asthma: A current perspective [Elektronische Daten] [Tony Bai] The role of the ß2-adrenergic receptor in both the pathogenesis and treatment of asthma has been a subject of intense speculation and investigation for 25 years. The physiological effects of endogenous circulating catecholamines and exogenous adrenergic agonists in the lung are mediated by the ß2-adrenergic receptor, which is present on a variety of cell types. Documented effects of ß2-adrenergic receptor activation in the human lung include smooth muscle relaxation, inhibition of acetylcholine release from cholinergic nerve terminals, stimulation of serous and mucous cell secretion, increases in ciliary beat frequency, promotion of water movement into the airway lumen by stimulation of ion secretion across the apical membrane of epithelial cells, increase in bronchial blood flow, reduction in venular permeability, and inhibition of mediator release from some, but not all, inflammatory cells. ß2-Adrenergic receptors are present in normal or increased numbers on asthmatic airway smooth muscle but are uncoupled in severe asthma, leading to functional hyporesponsiveness, probably due to the effects of inflammatory mediators. There is also evidence for dysfunction of ß2-adrenergic receptors on circulating inflammatory cells following mediator release. However, dysfunction of the receptors on airway smooth muscle and inflammatory cells is unlikely to be of primary importance in the pathogenesis of asthma. There is increasing concern that regular ß2-adrenergic receptor agonist use in the therapy of asthma is deleterious. Although a number of theories have been advanced to explain such an effect, none is well established and further research is urgently required. Springer-Verlag, 1992 Asthma nationallicence Beta2-adrenergic receptors nationallicence Asthma, pathogenesis nationallicence Asthma, treatment nationallicence Lung Springer-Verlag 170/3(1992-05-01), 125-141 0341-2040 170:3<125 1992 170 408 https://doi.org/10.1007/BF00174316 text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00174316 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Bai Tony Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, V6Z 1Y6, Vancouver, British Columbia, Canada aut NATIONALLICENCE 773 0- Lung Springer-Verlag 170/3(1992-05-01), 125-141 0341-2040 170:3<125 1992 170 408 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer