Contribution of the renin-angiotensin system in chronic foot-shock induced hypertension in rats.
Contribution of the renin-angiotensin system in chronic foot-shock induced hypertension in rats.
复制标题
DOI：
10.1016/j.lfs.2014.12.004
复制
发表时间：
2015-01
期刊：
影响因子：
6.1
通讯作者：
Lin-Hui Wang;Tao Dong;Bei-bei Liu;Xiao-Dong Zhao;Jing-Wei Chen;K. Murao;Wei Zhu;Guo-Xing Zhang
中科院分区：
文献类型：
--
作者：
Lin-Hui Wang;Tao Dong;Bei-bei Liu;Xiao-Dong Zhao;Jing-Wei Chen;K. Murao;Wei Zhu;Guo-Xing Zhang
目的 慢性足部休克已被证明可诱发高血压。本研究旨在探讨肾素-血管紧张素系统（RAS）是否在此过程中发挥作用以及慢性足休克诱发高血压的可能机制。主要方法对雄性Sprague-Dawley大鼠进行为期两周的足部休克，使用或不使用血管紧张素II（Ang II）1型受体阻滞剂（ARB，坎地沙坦）或血管紧张素I转换酶 抑制剂（ACEI、卡托普利）。检查了中枢神经和循环系统中 RAS 成分的表达。监测血浆中的抗氧化剂水平。主要发现两周的足部电击显着增加了收缩压（SBP）。大脑皮层和下丘脑血管紧张素原、血管紧张素I转换酶(ACE)-1、ACE-2、血管紧张素1a型和1b型受体、加压素(VAP) mRNA表达量随着血浆中肾素和Ang II浓度的增加而增加;这些变化伴随着谷胱甘肽过氧化物酶活性的降低以及脂质过氧化水平和血浆皮质酮浓度的增加。坎地沙坦和卡托普利不仅抑制收缩压的增加，而且抑制下丘脑中VAP表达的增加以及中枢神经系统和循环系统中RAS成分的增加。坎地沙坦或卡托普利治疗也部分逆转了抗氧化剂水平的降低以及脂质过氧化和皮质酮水平的增加。 意义慢性足休克增加了主要 RAS 成分的表达，这些成分通过增加 VAP 水平、氧化应激水平和应激激素水平在高血压的发展中发挥重要作用。
AimsChronic foot shock has been demonstrated to induce hypertension. The present study was designed to explore whether the renin–angiotensin system (RAS) plays a role in this process and the possible mechanisms involved in chronic-foot-shock-induced hypertension.Main methodsMale Sprague–Dawley rats were subjected to a two-week foot shock with or without an angiotensin II (Ang II) type 1 receptor blocker (ARB, candesartan) or an angiotensin I converting enzyme inhibitor (ACEI, captopril). The expression of RAS components in the central nervous and circulatory systems was examined. Antioxidant levels in the plasma were monitored.Key findingsTwo-week foot shock significantly increased systolic blood pressure (SBP). Angiotensinogen, angiotensin I converting enzyme (ACE)-1, ACE-2, angiotensin type 1a and type 1b receptors, and vasopressin (VAP) mRNA expression in the cerebral cortex and hypothalamus were increased along with the concentration of renin and Ang II in the plasma; these changes were accompanied by decreased glutathione peroxidase activity and increased lipid peroxidation levels and plasma corticosterone concentrations. Both candesartan and captopril suppressed not only the increases in SBP but also the increases in VAP expression in the hypothalamus and RAS components in the central nervous system and the circulatory system. The decreases in antioxidant levels and the increases in lipid peroxidation and corticosterone levels were also partially reversed by candesartan or captopril treatment.SignificanceChronic foot shock increases expression of the main RAS components, which play an important role in the development of high blood pressure through increased VAP levels, oxidative stress levels and stress hormone levels.