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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">arthyper</journal-id><journal-title-group><journal-title xml:lang="ru">Артериальная гипертензия</journal-title><trans-title-group xml:lang="en"><trans-title>"Arterial’naya Gipertenziya" ("Arterial Hypertension")</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1607-419X</issn><issn pub-type="epub">2411-8524</issn><publisher><publisher-name>Antihypertensive League</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18705/1607-419X-2003-9-1-14-16</article-id><article-id custom-type="elpub" pub-id-type="custom">arthyper-866</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>ОРИГИНАЛЬНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES</subject></subj-group></article-categories><title-group><article-title>Трансформирующий фактор-β1 и маркеры активации лейкоцитов при гипертонической болезни</article-title><trans-title-group xml:lang="en"><trans-title>Transforming factor-bl and markers of leukocytic activation in hypertensive disease</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Моисеева</surname><given-names>О. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Moiseyeva</surname><given-names>O. M.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лясникова</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Lyasnikova</surname><given-names>Ye. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Семенова</surname><given-names>Е. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Semenova</surname><given-names>E. G.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лопатенкова</surname><given-names>О. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Lopatenkova</surname><given-names>O. G.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шляхто</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shlyakhto</surname><given-names>Ye. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>НИИ кардиологии им. В.А.Алмазова Минздрава РФ, Санкт-Петербург</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2003</year></pub-date><pub-date pub-type="epub"><day>28</day><month>02</month><year>2003</year></pub-date><volume>9</volume><issue>1</issue><fpage>14</fpage><lpage>16</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Моисеева О.М., Лясникова Е.А., Семенова Е.Г., Лопатенкова О.Г., Шляхто Е.В., 2003</copyright-statement><copyright-year>2003</copyright-year><copyright-holder xml:lang="ru">Моисеева О.М., Лясникова Е.А., Семенова Е.Г., Лопатенкова О.Г., Шляхто Е.В.</copyright-holder><copyright-holder xml:lang="en">Moiseyeva O.M., Lyasnikova Y.A., Semenova E.G., Lopatenkova O.G., Shlyakhto 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://htn.almazovcentre.ru/jour/article/view/866">https://htn.almazovcentre.ru/jour/article/view/866</self-uri><abstract><p>Цель работы - определить концентрацию активной формы трансформирующего ростового фактора-ß1 (ТРФ-ß1 в сыворотке крови и функциональное состояние лейкоцитов у больных гипертонической болезнью (ГБ) II стадии. Оценить патогенетическое значение и возможность коррекции выявленных изменений с помощью ингибитора ангиотензинпревращающего фермента (АПФ) квинаприла. Обследованы 30 больных ГБ II стадии и 17 практически здоровых лиц. Оценивали данные ультразвукового исследования сердца, лучевой и сонных артерий, функциональную активность лейкоцитов и концентрацию ΤΡΦ-ßj в сыворотке крови. Из них 15 больных ГБ были обследованы повторно на фоне лечения квинаприлом (аккупро, "Pfizer", USA) в течение 12 нед в дозе 10-40 мг/сут. Установлено повышение уровня ΤΡΦ-ßj в сыворотке крови у больных ГБ и его связь с массой миокарда левого желудочка, толщиной комплекса интима-медиа общих сонных артерий и эндотелиальной дисфункцией. Показана связь между концентрацией ΤΡΦ-ßj и функциональной активностью лейкоцитов: увеличением числа лейкоцитов в периферической крови, адгезионной способностью нейтрофилов, экспрессией антиапоптотического белка Вс1-2 и Fas-рецепторов на лимфоцитах. В процессе лечения квинаприлом снижение исходного артериального давления на 10 мм рт. ст. и более у 87% больных сочеталось с уменьшением адгезии нейтрофилов к эндотелию, увеличением Bcl-2-негативных и Fas-позитивных лимфоцитов. Динамика уровня ΤΡΦ-ßj в сыворотке крови связана с поражением органов-мишеней и активацией лейкоцитов при ГБ. Снижение функциональной активности лейкоцитов на фоне терапии квинаприлом не зависело от антигипертензивного эффекта препарата.</p></abstract><trans-abstract xml:lang="en"><p>The study was undertaken to determine the serum concentration of an active form of transforming growth factor-bl (TGF-bl) and the functional status of leukocytes in patients with Stage II hypertensive disease (HD) and to assess the pathogenetic value and capacities of correction of detected changes with the angiotensin-converting enzyme (ACE) inhibitor quinapril. Materials and methods. Thirty patients with Stage II HD and 17 apparently healthy individuals were examined. The data of ultrasound studyofthe heart, radial and carotid arteries, the functional activity of leukocytes and the concentration of (TGF-bl) in the serum were assessed. Of them, 15 patients with HD were reexamined during treatment with quinapril (accupro, Pfizer, USA) in a daily dose of 10-40 mg for 12 weeks. Results. The study established an increase in the elevated serum levels of TGF-bl of hypertensive patients with HD and its association with the mass of the left ventricular myocardium, with the thickness of an intima-media complex of the common carotid arteries, and with endothelial dysfunction. A relationship is shown between the concentration of TGF-bl and the functional activity of leukocytes: elevated peripheral leukocytes, the adhesive capacity of neutrophils, the lymphocytic expression of the antiapoptic protein Bcl-2 and Fas-receptors. With quinapril treatment, a 10-mm Hg or more reduction in 87% of the patients was attended by the lower adhesion of neutrophils to the endothelium, with elevated Bcl-2-negative and Fas-positive lymphocytes. Conclusion. The changes in the serum levels of TGF-bl are associated with lesions of target organs and with the activation of leukocytes in HD. The decrease in leukocytic functional activity during therapy with quinapril did not depend on the antihypertensive effect of the drug.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>трансформирующий ростовой фактор-ßj</kwd><kwd>лейкоциты</kwd><kwd>гипертрофия левого желудочка</kwd><kwd>эндотелиальная дисфункция</kwd><kwd>квинаприл</kwd></kwd-group><kwd-group xml:lang="en"><kwd>transforming growth factor-bl</kwd><kwd>leukocytes</kwd><kwd>left ventricular hypertrophy</kwd><kwd>endothelial dysfunction</kwd><kwd>quinapril</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">Williams В. Angiotensin II and the pathophysiology oj cardiovascular remodeling. Am J Cardiol 2001; 87 (8A): 10C-17C.</mixed-citation><mixed-citation xml:lang="en">Williams В. Angiotensin II and the pathophysiology oj cardiovascular remodeling. 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