Ang(1-7)对高血压心脏重构的作用机制研究进展

Research progress in the mechanism of Ang(1-7)on cardiac remodeling in hypertensive patients

高血压正在成为威胁人类健康最常见的心血管疾病,可通过多种机制引起心室肥厚和心力衰竭。其中,肾素-血管紧张素-醛固酮系统(RAAS)激活是高血压心脏重构和充血性心力衰竭发生发展过程中的主要机制。已证明血管紧张素转换酶2(ACE2)和血管紧张素(Ang)(1-7)是RAAS的主要组成部分。本文以上述研究为背景,就Ang(1-7)对慢性压力负荷下心脏重构的保护作用展开综述。

Hypertension is the most common risk factor for cardiovascular disease and can promote cause ventricular hypertrophy and heart failure through various mechanisms.Among them,renin-angiotensin aldosterone system(RAAS)activation is the main mechanism for the pathology of hypertensive heart remodeling and heart failure.Angiotensin converting enzyme 2 and Ang(1-7)have been shown to be major components of RAAS.Based on the above studies,this paper reviews the protective effects of Ang(1-7)on cardiac remodeling under chronic stress.