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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">rpcardio</journal-id><journal-title-group><journal-title xml:lang="en">Rational Pharmacotherapy in Cardiology</journal-title><trans-title-group xml:lang="ru"><trans-title>Рациональная Фармакотерапия в Кардиологии</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1819-6446</issn><issn pub-type="epub">2225-3653</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.20996/1819-6446-2024-3067</article-id><article-id custom-type="elpub" pub-id-type="custom">rpcardio-3067</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="en"><subject>ORIGINAL STUDIES</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group></article-categories><title-group><article-title>The effect of the M235T polymorphism of the angiotensinogen gene on the office blood pressure during therapy with angiotensin II receptor blockers</article-title><trans-title-group xml:lang="ru"><trans-title>Влияние полиморфизма M235T гена ангиотензиногена на офисное артериальное давление на фоне терапии блокаторами рецепторов ангиотензина II</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4374-9754</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Реброва</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Rebrova</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Реброва Екатерина Владиславовна, доцент кафедры клинической фармакологии и пропедевтики внутренних болезней, к.м.н.</p><p> </p></bio><bio xml:lang="en"><p>Ekaterina V. Rebrova </p><p> Moscow </p></bio><email xlink:type="simple">katrina1987@rambler.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6589-7654</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ших</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shikh</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ших Евгения Валерьевна, зав. кафедрой клинической фармакологии и пропедевтики внутренних болезней, д.м.н., профессор</p></bio><bio xml:lang="en"><p>Evgeniya V. Shikh </p><p>Moscow </p></bio><email xlink:type="simple">chih@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 «Первый МГМУ им. И. М. Сеченова» (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Sechenov First Moscow State Medical University (Sechenov University)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>24</day><month>10</month><year>2024</year></pub-date><volume>20</volume><issue>5</issue><fpage>506</fpage><lpage>513</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Rebrova E.V., Shikh E.V., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Реброва Е.В., Ших Е.В.</copyright-holder><copyright-holder xml:lang="en">Rebrova E.V., Shikh E.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://www.rpcardio.online/jour/article/view/3067">https://www.rpcardio.online/jour/article/view/3067</self-uri><abstract><p>Aim. To study the pharmacodynamic parameters of the effectiveness of therapy with angiotensin II receptor blockers in the form of monotherapy and as part of combination drugs in patients with hypertension, depending on the genetic characteristics of patients — the M235T polymorphism of the angiotensinogen gene (AGT).Material and methods. The study included 179 patients in the Moscow region with newly diagnosed hypertension of 1-2 degrees, among whom 141 (78.8%) women and 38 (21.2%) men aged 32 to 69 years, who were randomly assigned to irbesartan and valsartan groups in the form of mono- or combination therapy with hydrochlorothiazide by a simple randomization method. After 3 weeks of pharmacotherapy, the presence of rs699 (C4072T, M235T) genetic polymorphism of the AGT was determined.Results. Homozygotes СС with the genetic polymorphism M235T of the AGT treated with valsartan had a statistically significantly higher frequency of achieving target blood pressure figures after 3 weeks of pharmacotherapy compared with TT homozygotes (p=0.006) and a statistically significantly lower frequency of the need to increase the dose of the drug compared with heterozygotes and TT homozygotes (p=0.047 and 0.006, respectively). Among patients treated with irbesartan, there was no statistically significant association of the M235T polymorphism genotype of the AGT with these indicators.Conclusion. The data obtained may indicate a faster and more stable antihypertensive effect in homozygotes of CC and TT of the genetic polymorphism M235T of the AGT. When personalizing hypertension therapy for patients of the Moscow region, carriers of homozygous CC and TT genotypes of the M235T genetic polymorphism of the AGT for more effective achievement of target blood pressure figures, it is advisable to recommend valsartan as a starting therapy in the form of mono- or twocomponent therapy, depending on the degree of hypertension.</p></abstract><trans-abstract xml:lang="ru"><p>Цель. Изучить фармакодинамические показатели эффективности терапии блокаторами рецепторов ангиотензина II в виде монотерапии и в составе комбинированных препаратов у пациентов с артериальной гипертензией (АГ) в зависимости от генетических особенностей — полиморфизма M235T гена ангиотензиногена (AGT).Материал и методы. В исследование включено 179 пациентов Московского региона с впервые выявленной АГ 1-2 степени, среди которых 141 (78,8%) женщины и 38 (21,2%) мужчины в возрасте от 32 до 69 лет, которые были случайным образом (методом простой рандомизации) распределены в группы ирбесартана и валсартана в виде моно- или комбинированной терапии с гидрохлортиазидом. Через 3 недели терапии определяли наличие генетического полиморфизма rs699 (C4072T, M235T) гена AGT.Результаты. Гомозиготы СС генетического полиморфизма M235T гена AGT, получавшие валсартан, имели статистически значимо более высокую частоту достижения целевых цифр АД через 3 недели терапии по сравнению с гомозиготами ТТ (p=0,006) и статистически значимо меньшую частоту потребности увеличения дозы препарата по сравнению с гетерозиготами и гомозиготами ТТ (p=0,047 и 0,006, соответственно). Среди пациентов, получавших ирбесартан, статистически значимой ассоциации генотипа полиморфизма M235T гена AGT с данными показателями выявлено не было.Заключение. Полученные данные могут свидетельствовать о более быстром и стабильном антигипертензивном эффекте у гомозигот СС и ТТ генетического полиморфизма M235T гена AGT. При персонализации терапии АГ пациентам Московского региона, носителям гомозиготных генотипов СС и ТТ генетического полиморфизма М235Т гена AGT для более эффективного достижения целевых цифр артериального давления целесообразно рекомендовать в качестве стартовой терапии блокатор рецепторов ангиотензина валсартан в виде моно- или двухкомпонентной терапии в зависимости от степени АГ.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>артериальная гипертензия</kwd><kwd>ген ангиотензиногена</kwd><kwd>полиморфизм M235T</kwd><kwd>ирбесартан</kwd><kwd>валсартан</kwd><kwd>офисное  артериальное давление</kwd><kwd>блокаторы рецепторов ангиотензина II</kwd></kwd-group><kwd-group xml:lang="en"><kwd>arterial hypertension</kwd><kwd>angiotensinogen gene</kwd><kwd>M235T polymorphism</kwd><kwd>irbesartan</kwd><kwd>valsartan</kwd><kwd>office blood pressure</kwd><kwd>angiotensin II receptor blockers</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена при поддержке Первого Московского медицинского университета им. 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