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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Telmisartan reduces atrial arrhythmia susceptibility through the regulation of RAS-ERK and PI3K-Akt-eNOS pathways in spontaneously hypertensive rats
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Telmisartan reduces atrial arrhythmia susceptibility through the regulation of RAS-ERK and PI3K-Akt-eNOS pathways in spontaneously hypertensive rats

机译：替米沙坦通过调节自发性高血压大鼠的RAS-ERK和PI3K-Akt-eNOS途径降低房性心律失常敏感性

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摘要

Telmisartan is an angiotensin II receptor blocker that displays unique PPAR-gamma modulating activity. PPAR-gamma agonists have been shown to decrease susceptibility to atrial fibrillation through their antioxidant and antiapoptotic effects. The aim of this study was to determine whether telmisartan would have a greater effect on susceptibility to atrial arrhythmia in a hypertensive rat model than valsartan, which is a traditional angiotensin II receptor blocker. In this study, spontaneously hypertensive rats were treated with 10 mg.(kg body mass)(-1).d(-1) telmisartan (TEL group), 10 mg.(kg body mass)(-1).d(-1) valsartan (VAL group), or vehicle (saline; SHR group) for 4 weeks. Age-matched Wistar-Kyoto rats (WKY) were used as normotensive controls. After 4 weeks of treatment, we performed echocardiographic assessment, electrophysiological analysis, histological evaluation, and Western blot analysis. Telmisartan decreased systolic blood pressure to a similar extent as valsartan. Relative to the WKY controls, atrial arrhythmia susceptibility was significantly increased in the SHR group, and was significantly decreased by both telmisartan and valsartan, albeit to a greater extent with telmisartan. Arrhythmogenic atrial remodeling, including enlargement of the left atrium, myocyte hypertrophy, interstitial fibrosis, and myocyte apoptosis, was observed in the SHR group, and was accompanied by activated RAS-ERK signaling and suppressed PI3K-Akt-eNOS signaling. The results suggest that telmisartan reduced susceptibility to atrial arrhythmia to a greater extent than valsartan, ameliorated atrial remodeling, and reversed imbalances in the RAS-ERK and PI3K-Akt-eNOS pathways.
机译：替米沙坦是一种血管紧张素II受体阻滞剂，具有独特的PPAR-γ调节活性。研究表明，PPAR-γ激动剂通过其抗氧化剂和抗凋亡作用降低对房颤的敏感性。这项研究的目的是确定替米沙坦在高血压大鼠模型中是否比传统的血管紧张素II受体阻滞剂缬沙坦对心律失常的敏感性更大。在这项研究中，自发性高血压大鼠用替米沙坦10 mg。（kg体重）（-1）.d（-1）（tel组），10 mg。（kg体重）（-1）.d（-）治疗1）缬沙坦（VAL组）或媒介物（盐水; SHR组）持续4周。使用年龄匹配的Wistar-Kyoto大鼠（WKY）作为血压正常对照。治疗4周后，我们进行了超声心动图评估，电生理分析，组织学评估和蛋白质印迹分析。替米沙坦降低收缩压的程度与缬沙坦相似。相对于WKY对照，SHR组的房性心律失常易感性显着增加，替米沙坦和缬沙坦均显着降低，尽管替米沙坦更大。在SHR组中观察到心律失常性心房重构，包括左心房增大，心肌肥大，间质纤维化和心肌细胞凋亡，并伴有激活的RAS-ERK信号传导和PI3K-Akt-eNOS信号传导抑制。结果表明，替米沙坦比缬沙坦更大程度地降低了对心律失常的敏感性，改善了心房重构，并逆转了RAS-ERK和PI3K-Akt-eNOS途径的失衡。

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