首页> 美国卫生研究院文献>Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease >Cardiac and Renal Protective Effects of Irbesartan via Peroxisome Proliferator‐Activated Receptorγ–Hepatocyte Growth Factor Pathway Independent of Angiotensin II Type 1a Receptor Blockade in Mouse Model of Salt‐Sensitive Hypertension
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Cardiac and Renal Protective Effects of Irbesartan via Peroxisome Proliferator‐Activated Receptorγ–Hepatocyte Growth Factor Pathway Independent of Angiotensin II Type 1a Receptor Blockade in Mouse Model of Salt‐Sensitive Hypertension

机译:厄贝沙坦通过过氧化物酶体增殖物激活的受体γ-肝细胞生长因子通路对血管紧张素Ⅱ1a受体阻滞的心脏和肾脏保护作用在盐敏感性高血压小鼠模型中

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摘要

Background“Aldosterone breakthrough” observed in patients receiving long‐term treatment with angiotensin blockade is strongly associated with increased risk of left ventricular hypertrophy, poor exercise capacity, refractory proteinuria, and declining glomerular filtration rate through the profibrotic actions of aldosterone. To overcome aldosterone breakthrough, we examined the additional organ‐protective actions of irbesartan, because irbesartan is an angiotensin II type 1 receptor (AT1R) blocker (ARB) with peroxisome proliferator‐activated receptor >(PPAR)γ agonistic effects, which mediate organ‐protective effects independent of AT1R blockade. In this study, we examined the organ‐protective effects of irbesartan in a salt‐sensitive hypertension model using AT1aR knockout mice.
机译:背景:长期接受血管紧张素阻滞治疗的患者中观察到的“醛固酮突破”与左室肥大,运动能力差,难治性蛋白尿以及通过醛固酮的纤维化作用降低肾小球滤过率的风险增加密切相关。为了克服醛固酮的突破,我们检查了厄贝沙坦的其他器官保护作用,因为厄贝沙坦是一种血管紧张素II 1型受体(AT1R)阻断剂(ARB),具有过氧化物酶体增殖物激活受体>( PPAR)γ激动剂介导的器官保护作用,独立于AT1R阻断作用。在这项研究中,我们使用AT1aR基因敲除小鼠研究了厄贝沙坦在盐敏感性高血压模型中的器官保护作用。

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