Arterial hypertension in metabolic syndrome: Pathophysiological aspects


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Abstract

Arterial hypertension (AH) is one of the basic components of metabolic syndrome that is caused by four factors: autonomic sympathetic dysfunction; activation of the hypothalamic-pituitary-adrenal axis; that of the renin-angiotensin-aldosterone system; and endothelial dysfunction (ED). AH is a slowly progressive hemodynamic disease, the natural course of which is characterized by not only elevated blood pressure (BP), but also by left ventricular hypertrophy, arterial remodeling, and a progressive increase in total peripheral resistance. ED and arterial remodeling play a key role in the pathogenesis of AH in metabolic syndrome. Remodeling of resistant arteries raises peripheral resistance and stabilizes BP and that of large arteries increases their stiffness and a reflected wave, resulting in increased pulse BP, systolic BP, and enhanced left ventricular hypertrophy. Insulin resistance and hyperinsulinemia increase the activity of the renin-angiotensin-aldosterone system and, by enhancing the expression of angiotensinogen, angiotensin II and its type 1 receptors, favors the development of AH, proinflammation, atherosclerosis, and congestive heart failure. Hyperleptinemia, which, by stimulating the activity of the sympathetic nervous system, elevates BP, plays a certain role in the development of AH in metabolic syndrome and obesity.

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Патофизиологические аспекты артериальной гипертонии при метаболическом синдроме. - Аннотация. Артериальная гипертония (АГ) - один из основных компонентов метаболического синдрома, развитие которого обусловлено четырьмя факторами: автономной дисфункцией симпатической части вегетативной нервной системы (С-ВНС), активацией гипоталамо-питуитрино-адреналовой и ренин-ангиотензин-альдостероновой систем, а также дисфункцией эндотелия (ДЭ). АГ - медленно прогрессирующее гемодинамическое заболевание, естественное течение которого характеризуется не только повышением артериального давления (АД), но также развитием гипертрофии левого желудочка (ГЛЖ), ремоделированием артерий и прогрессивным повышением общего периферического сопротивления. В патогенезе АГ при метаболическом синдроме ключевая роль принадлежит ДЭ и ремоделированию артерий. Ремоделирование резистивных артерий увеличивает периферическое сопротивление и стабилизирует АД, а ремоделирование крупнокалиберных артерий повышает жесткость артерий и увеличивает отраженную волну, в результате чего повышается пульсовое АД, систолическое АД и усиливается ГЛЖ. Инсулинорезистентность и гиперинсулинемия повышают активность ренин-ангиотензин-альдостероновой системы и, усиливая экспрессию ангиотензиногена, ангиотензина II и его рецепторов 1-го типа (АТ1-рецепторов), способствуют развитию АГ, провоспаления, атеросклероза и застойной сердечной недостаточности. В развитии АГ при метаболическом синдроме и ожирении определенную роль играет гиперлептинемия, которая стимулируя активность С-ВНС, повышает АД.
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