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ИНАКТИВАЦИЯ РЕНИН-АНГИОТЕНЗИН-АЛЬДОСТЕРОНОВОЙ СИСТЕМЫ. КАКОЙ КЛАСС ПРЕПАРАТОВ ПРЕДПОЧЕСТЬ?

https://doi.org/10.38109/2225-1685-2020-4-64-78

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Аннотация

Представлен сравнительный анализ эффективности двух классов лекарственных препаратов – ингибиторов ангиотензинпревращающего фермента (ИАПФ) и блокаторов  рецептора 1 типа ангиотензина II (БРА II) в профилактике сердечно-сосудистых заболеваний. Показано преимущество ИАПФ перед БРА II в снижении общей и  кардиоваскулярной смертности, инфарктов миокарда, мозговых инсультов, хронической сердечной недостаточности, хронической болезни почек. Причины различного влияния  ингибиторов ренин-ангиотензинальдостероновой системы на течение  кардиоваскулярной патологии объясняются механизмами терапевтического воздействия ИАПФ и БРА II. Антигипертензивное действие БРА II обеспечивается селективной  блокадой АТ1-¬рецепторов к ангиотензину II (АТ II). В результате блокады в крови накапливается дополнительное количество АТ II, который связываясь с АТ2- рецепторами, способствует появлению ряда негативных явлений. Стимуляция АТ2-рецепторов (возможно также АТ3-, АТ4-рецепторов) неутилизированным АТ II приводит к апоптозу структурных элементов артериальной стенки, её фиброзу, склерозированию  и гипертрофии, торможению коронарного ремоделирования с нарушением  неоваскуляризации миокарда, а также усилению проатерогенных и воспалительных процессов в эндотелии, возможно и сердечной ткани. Стимуляция АТ2-рецепторов также способствует лейкоцитзависимому высвобождению матриксной металлопротеиназы I,  которая приводит к деструкции белков внеклеточного матрикса, тем самым дестабилизируя атеросклеротическую бляшку, приводя к ее разрыву, что является возможной причиной увеличения риска инфаркта миокарда при лечении сартанами. Каскад этих негативных влияний может быть основным механизмом дестабилизации ИБС при назначении БРА II. В отличие от сартанов лечебный потенциал ИАПФ реализуется через блокаду синтеза АТ II, не влияя на работу рецепторного аппарата, поэтому  вышеуказанных неблагоприятных эффектов, связанных с накоплением АТ II, не  происходит. Важной физиологической особенностью ИАПФ является их способность  повышать уровень брадикинина, который оказывает положительное влияние на стенку сосудов, снижает их жесткость путем увеличения синтеза простагландинов,  демонстрирует антиоксидантный и антиапоптотический эффекты, приводит к снижению  постнагрузки и стимуляции ангиогенеза. Именно эти механизмы лежат в основе более выраженного кардиопротективного действия ИАПФ в отличие от БРА II.

Об авторе

С. В. Столов
ФГБУ ДПО «Санкт-Петербургский институт усовершенствования врачей-экспертов» Минтруда России; ФГБУ ВО «Северо-Западный государственный медицинский университет»
Россия

д.м.н., заведующий кафедрой терапии, МСЭ и реабилитации №1; профессор кафедры терапии и ревматологии им. Э.Э. Эйхвальда

sv100lov@gmail.com

194044, Г. Санкт-Петербург, Большой Сампсониевский Пр., Д. 11/12

191015, Г. Санкт-Петербург, Ул. Кирочная, Д. 41



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Для цитирования:


Столов С.В. ИНАКТИВАЦИЯ РЕНИН-АНГИОТЕНЗИН-АЛЬДОСТЕРОНОВОЙ СИСТЕМЫ. КАКОЙ КЛАСС ПРЕПАРАТОВ ПРЕДПОЧЕСТЬ? Евразийский кардиологический журнал. 2020;(4):64-78. https://doi.org/10.38109/2225-1685-2020-4-64-78

For citation:


Stolov S.V. INACTIVATION OF RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM. WHICH CLASS OF ANTIHYPERTENSIVE MEDICINE PRODUCTS TO PREFER? Eurasian heart journal. 2020;(4):64-78. (In Russ.) https://doi.org/10.38109/2225-1685-2020-4-64-78

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