Journal of Clinical PracticeJournal of Clinical PracticeКлиническая практика2220-30952618-8627Eco-Vector3513410.17816/clinpract35134ReviewsНаучные обзорыReview ArticleBeta-adrenergic and M-cholinergic receptor interactions in the pathogenesis of bronchial obstructive pulmonary diseasesОсобенности рецепторных взаимодействий бета-адренергической и М-холинергической систем в патогенезе развития бронхообструктивных заболеванийhttps://orcid.org/0000-0001-9333-00222813-1638EremenkoAnna V.ЕременкоАнна Владимировна
Russian Federation
a_nn87@list.ru6269-7990ZykovKirill A.ЗыковКирилл Алексеевич
Russian Federation

MD, PhD, Professor

д.м.н., профессор РАН

kirillaz@inbox.ruResearch Institute of Pulmonology of the Federal Medical and Biological Agency of RussiaНаучно-исследовательский институт пульмонологии Федерального медико-биологического агентства РоссииMoscow State University of Medicine and Dentistry named after A.I. EvdokimovМосковский государственный медико-стоматологический университет им. А.И. Евдокимова140920202310202011368741007202002092020Copyright ©; 2020, Eremenko A.V., Zykov K.A.Copyright ©; 2020, Еременко А.В., Зыков К.А.2020Eremenko A.V., Zykov K.A.Еременко А.В., Зыков К.А.https://creativecommons.org/licenses/by-nc-nd/4.0https://clinpractice.ru/clinpractice/article/view/35134

The crosstalk between the beta-2-adrenoceptor and M- cholinoreceptor systems in the airways plays one of the main roles in the pathogenesis of bronchoobstructive diseases. The interaction of M3-cholinergic receptors and beta2-receptors in the lungs can be characterized as functional antagonism. M3 activation can lead to desensitization of beta2 receptors. Beta2 receptors also limit the action of M3 receptors in various ways. In this case, M2 cholinergic receptors act as autoreceptors. On the one hand, they limit bronchoconstriction caused by a change in the conformation of the M3 cholinergic receptor, and, on the other hand, they are able to suppress the excessive bronchorelaxing effect that occurs when a beta2 receptor is activated. The knowledge of the crosstalk mechanisms can help in understanding the pathogenesis of bronchial obstructive diseases, in optimizing the existing treatment regimens for chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA) and will create a new potential in the development of new drug groups

Одну из ведущих ролей в патогенезе бронхообструктивной патологии играет взаимодействие бета-адренергической и М-холинергической рецепторных систем. Взаимодействие М3-холинорецепторов и бета2-рецепторов в легких можно охарактеризовать как функциональный антагонизм. Активация М3 способна приводить к десенситизации бета2-рецепторов, которые в свою очередь также ограничивают действие М3-рецепторов различными способами. При этом М2-холинорецепторы выступают в роли ауторецепторов. С одной стороны, они ограничивают бронхоконстрикцию, вызванную изменением конформации М3-холинорецептора, с другой — способны подавлять избыточный бронхорелаксирующий эффект, возникающий при активации бета2-рецептора. Понимание механизмов данных взаимодействий поможет объяснить патогенез бронхообструктивных заболеваний, оптимизировать существующие схемы терапии хронической обструктивной болезни легких и бронхиальной астмы, откроет возможности для разработки новых групп препаратов.

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