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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Consilium Medicum</journal-id><journal-title-group><journal-title xml:lang="en">Consilium Medicum</journal-title><trans-title-group xml:lang="ru"><trans-title>Consilium Medicum</trans-title></trans-title-group><trans-title-group xml:lang="zh"><trans-title>Consilium Medicum</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-1753</issn><issn publication-format="electronic">2542-2170</issn><publisher><publisher-name xml:lang="en">Consilium Medicum</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">92369</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Antagonisty retseptorov angiotenzina II v poiskakh «farmakologicheskoy nishi»</article-title><trans-title-group xml:lang="ru"><trans-title>Антагонисты рецепторов ангиотензина II в поисках «фармакологической ниши»</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Perepech</surname><given-names>N. B</given-names></name><name xml:lang="ru"><surname>Перепеч</surname><given-names>Н. Б</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">ГОУ ВПО Санкт-Петербургская государственная медицинская академия им. И.И.Мечникова</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2007-05-15" publication-format="electronic"><day>15</day><month>05</month><year>2007</year></pub-date><volume>9</volume><issue>5</issue><issue-title xml:lang="en">VOL 9, NO5 (2007)</issue-title><issue-title xml:lang="ru">ТОМ 9, №5 (2007)</issue-title><fpage>36</fpage><lpage>44</lpage><history><date date-type="received" iso-8601-date="2021-12-28"><day>28</day><month>12</month><year>2021</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2007, Consilium Medicum</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2007, ООО "Консилиум Медикум"</copyright-statement><copyright-year>2007</copyright-year><copyright-holder xml:lang="en">Consilium Medicum</copyright-holder><copyright-holder xml:lang="ru">ООО "Консилиум Медикум"</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by-nc-sa/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://consilium.orscience.ru/2075-1753/article/view/92369">https://consilium.orscience.ru/2075-1753/article/view/92369</self-uri><abstract xml:lang="ru"><p>Прогрессирование сердечно-сосудистых заболеваний – от факторов риска до развития фатальных осложнений – связано с нарастанием активности ренин-ангиотензин-альдостероновой системы (РААС). Хроническая гиперактивация РААС проявляется увеличением содержания в крови и тканях ее главного эффекторного пептида – ангиотензина II. К числу основных физиологических эффектов ангиотензина II относятся вазоконстрикция, усиление синтеза и секреции альдостерона, задержка натрия и воды, повышение тонуса симпатической нервной системы, усиление высвобождения вазопрессина, эндотелина-1 и норадреналина, стимуляция роста кардиомиоцитов и клеток соединительной ткани в миокарде, пролиферации гладкомышечных клеток и фибробластов в сосудистой стенке, а также мезангиальных клеток в почечных клубочках. Повреждающее воздействие ангиотензина II на органы-мишени выражается в развитии гипертрофии миокарда и миокардиофиброза, прогрессировании атеросклероза, повышении внутриклубочкового давления с последующим развитием нефросклероза, патологической цереброваскулярной реконструкции. Результаты выполненных экспериментальных и клинических исследований позволяют считать повышение уровня ангиотензина II независимым фактором риска сердечно-сосудистых заболеваний</p></abstract></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Brunner H.R. Experimental and clinical evidence that angiotensin II is an independent risk factor for cardiovascular disease. Am J Cardiol 2001; 87: 3C–9C.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Cuspidi C, Muiesan M.L, Valagussa L et al. Comparative effects of candesartan and enalapril on left ventricular hypertrophy in patients with essential hypertension: the Сandesartan Assessment in the Treatment of Cardiac Hypertrophy (CATCH) study. J Hypertens 2002; 20: 2293–300.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Himmelmann A, Keinanen-Kiukaanniemi S, Wester A et al. 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