Angiotensin (1-7) Alleviates Postresuscitation Myocardial Dysfunction by Suppressing Oxidative Stress Through the Phosphoinositide 3-Kinase, Protein Kinase B, and Endothelial Nitric Oxide Synthase Signaling Pathway

血管紧张素II 一氧化氮 一氧化氮合酶 内科学 氧化应激 内分泌学 医学 蛋白激酶A 激酶 化学 药理学 受体 生物化学
作者
Li Zhu,Zhen Liu,Liping Huang,Hourong Zhou,Yu Cao,Xueping Yang,Bingjin Wang,Zi-li Yang,Jing Chen
出处
期刊:Journal of Cardiovascular Pharmacology [Ovid Technologies (Wolters Kluwer)]
卷期号:78 (1): e65-e76 被引量:4
标识
DOI:10.1097/fjc.0000000000001037
摘要

Abstract: There is increasing evidence that angiotensin (1-7) [Ang (1-7)] is an endogenous biologically active component of the renin–angiotensin system. However, the role of the Ang (1-7)-MasR axis in postresuscitation myocardial dysfunction (PRMD) and its associated mechanism are still unclear. In this study, we investigated the effect of the Ang (1-7)-MasR axis on myocardial injury after cardiac arrest-cardiopulmonary resuscitation-restoration of spontaneous circulation. We established a model of oxygen/glucose deprivation-reperfusion in myocardial cells in vitro and a rat model of cardiac arrest–cardiopulmonary resuscitation–restoration of spontaneous circulation in vivo. The cell apoptosis rate and the expression of the superoxide anion 3-nitrotyrosine were decreased in the Ang (1-7) group in vitro and in vivo. The mean arterial pressure was decreased, whereas +LVdp/dtmax and −LVdp/dtmax were increased in rats in the Ang (1-7) group. The mRNA and protein levels of Ang II type 1 receptor, MasR, phosphoinositide 3-kinase, protein kinase B, and endothelial nitric oxide synthase were increased in the Ang (1-7) group in vivo. These results indicate that the Ang (1-7)-MasR axis can alleviate PRMD by reducing myocardial tissue damage and oxidative stress through activation of the phosphoinositide 3-kinase–protein kinase B–endothelial nitric oxide synthase signaling pathway and provide a new direction for the clinical treatment of PRMD.
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