Beta-agonist: Bronchodilation mechanism
Last updated: 05/31/2017
Bronchodilation due to administration of beta-agonists is specifically related to their action at the β2-adrenoceptors. The efficacy of β2-agonists for patients with asthma and COPD results from a direct relaxation of airway smooth muscle and a secondary reduction of inflammatory cell activation. β2-stimulation results in bronchodilation due to multiple downstream signaling mechanisms within airway smooth muscle cells that all favor relaxation. β2-adrenoceptors are coupled with the stimulatory G protein (Gs ), which activates membrane-associated adenylyl cyclase to produce the second messenger cAMP. The intracellular increase of cAMP leads to the activation of several targets, including protein kinase A. Activation of protein kinase A (pkA) leads to the opening of Ca2+ activated K+ channels with efflux of calcium out of the cell and into the sarcoplasmic reticulum with resulting plasma membrane hyperpolarization. There is also decreased intracellular entry of Ca2+, and a decrease in the sensitivity of the contractile proteins to Ca2+. All of these effects culminate in the relaxation of airway smooth muscle cells.
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