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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">russjcardiol</journal-id><journal-title-group><journal-title xml:lang="ru">Российский кардиологический журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Russian Journal of Cardiology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1560-4071</issn><issn pub-type="epub">2618-7620</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15829/1560-4071-2023-5681</article-id><article-id custom-type="edn" pub-id-type="custom">RDLHIH</article-id><article-id custom-type="elpub" pub-id-type="custom">russjcardiol-5681</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>КЛИНИКА И ФАРМАКОТЕРАПИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>GUIDELINES FOR THE PRACTITIONER</subject></subj-group></article-categories><title-group><article-title>Современные представления о последствиях гиперактивации симпатоадреналовой системы у больных артериальной гипертонией с метаболическими нарушениями: возможности модуляции</article-title><trans-title-group xml:lang="en"><trans-title>Modern ideas about the consequences of sympathoadrenal hyperactivation in hypertensive patients with metabolic disorders: modulation possibilities</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7895-9068</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Жернакова</surname><given-names>Ю. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Zhernakova</surname><given-names>Yu. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Д. м. н., профессор кафедры кардиологии; ученый секретарь, Институт клинической кардиологии им. А.Л. Мясникова</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">juli001@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГАОУ ВО РНИМУ им. Н.И. Пирогова Минздрава России; &#13;
ФГБУ НМИЦ кардиологии им. акад. И.Е. Чазова Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>N.I. Pirogov Russian National Research Medical University; &#13;
I.E. Chazov National Medical Research Center of Cardiology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>19</day><month>12</month><year>2023</year></pub-date><volume>28</volume><issue>12</issue><fpage>5681</fpage><lpage>5681</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Жернакова Ю.В., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Жернакова Ю.В.</copyright-holder><copyright-holder xml:lang="en">Zhernakova Y.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://russjcardiol.elpub.ru/jour/article/view/5681">https://russjcardiol.elpub.ru/jour/article/view/5681</self-uri><abstract><p>Распространенность артериальной гипертонии (АГ) в Российской Федерации и в мире в целом продолжает расти. В немалой степени это связано с эпидемией ожирения и ассоциированных с ним состояний — метаболического синдрома и сахарного диабета (СД) 2 типа. Наиболее распространенной и доказанной гипотезой взаимосвязи АГ и ожирения является активация симпатической нервной системы (СНС). Вместе с тем современные исследования показывают, что последствия гиперактивации СНС не ограничиваются только гемодинамическими эффектами, а распространяются на многие органы и системы. Если симпатическая активность повышена длительно — это может привести к развитию инсулинорезистентности и СД 2 типа. Нейротрансмиттеры влияют на жировые клетки, усиливая липолиз и приводя к увеличению выделения жирных кислот, на печень, увеличивая глюконеогенез, на β-клетки поджелудочной железы, снижая секрецию инсулина. СНС играет важную роль в управлении энергией посредством регуляции скорости метаболизма. У лиц с ожирением значительно менее выражен постпрандиальный термогенез, несмотря на более высокий инсулиновый ответ, снижен гемодинамический ответ на изометрические или гетерометрические упражнения. Хронический стресс, который является одним из составляющих синдрома ожирения, служит не только триггером, приводящим к поведенческим нарушениям, но и напрямую приводит к срыву различных физиологических систем, в т.ч. через активацию СНС. Однако выбор антигипертензивных препаратов, влияющих на активность СНС у больных с ожирением и метаболическими нарушениями, весьма ограничен. Согласно текущим рекомендациям, β-блокаторы не являются препаратами выбора у больных неосложненной АГ, в связи с тем, что они имеют меньшую доказательную базу, по сравнению с другими классами препаратов и обладают метаболическими и другими побочными эффектами. Учитывая это, селективные агонисты I1-имидазолиновых рецепторов и, в частности моксонидин, могут быть препаратами выбора у этой категории больных. Использование моксонидина в комбинированной терапии пациентов с АГ и метаболическими нарушениями, в т.ч. с менопаузальным метаболическим синдромом, а также с физиологическим снижением уровня эстрогенов значительно улучшает эффективность антигипертензивной терапии, повышает вероятность достижения целевых уровней артериального давления, а воздействие на метаболические процессы сопровождается улучшением прогноза у данной категории больных.</p></abstract><trans-abstract xml:lang="en"><p>The prevalence of hypertension (HTN) in the Russian Federation and the world continues to grow. This is largely due to the epidemic of obesity and related conditions — metabolic syndrome and type 2 diabetes. The most common and proven hypothesis of the relationship between hypertension and obesity is the activation of the sympathetic nervous system. However, modern research shows that the consequences of sympathetic hyperactivation are not limited only to hemodynamic effects, but extend to many organs and systems. Long-term sympathetic hyperactivation can lead to insulin resistance and type 2 diabetes. Neurotransmitters affect fat cells by increasing lipolysis and leading to increased fatty acid release, the liver by increasing gluconeogenesis, and pancreatic β-cells by decreasing insulin secretion. The sympathetic nervous system plays an important role in energy management by regulating metabolic rate. Obese individuals have significantly less pronounced postprandial thermogenesis, despite a higher insulin response, while the hemodynamic response to isometric or heterometric exercise is reduced. Chronic stress serves not only as a trigger for behavioral disorders, but also directly leads to various physiological disorders, including through sympathetic activation. However, the choice of antihypertensive agents affecting the sympathetic activity in patients with obesity and metabolic disorders is very limited. According to current guidelines, β-blockers are not the drugs of choice in patients with uncomplicated HTN, since it has a weaker evidence base compared to other classes of drugs and have metabolic and other side effects. Therefore, selective I1-imidazoline receptor agonists, and in particular, moxonidine may be the drugs of choice in this category of patients. Moxonidine in combination therapy of patients with HTN and metabolic disorders, including metabolic disorders in menopause, as well as with a physiological estrogen decrease, significantly improves the effectiveness of antihypertensive therapy and increases the achievement of target blood pressure. In addition, its metabolic effects improve prognosis of such patients.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>метаболический синдром</kwd><kwd>симпатическая нервная система</kwd><kwd>артериальная гипертония</kwd><kwd>ожирение</kwd><kwd>моксонидин</kwd><kwd>менопауза</kwd></kwd-group><kwd-group xml:lang="en"><kwd>metabolic syndrome</kwd><kwd>sympathetic nervous system</kwd><kwd>hypertension</kwd><kwd>obesity</kwd><kwd>moxonidine</kwd><kwd>menopause</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Kalil GZ, Haynes WG. Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications. Hypertens Res. 2012;35(1):4-16.</mixed-citation><mixed-citation xml:lang="en">Kalil GZ, Haynes WG. Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications. 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