• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >ANG II-induced cardiac molecular and cellular events: role of aldosterone.
【24h】

ANG II-induced cardiac molecular and cellular events: role of aldosterone.

机译：ANG II诱导的心脏分子和细胞事件：醛固酮的作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chronic elevation of circulating ANG II is associated with cardiac remodeling in patients with hypertension and heart failure. The underlying mechanisms, however, are not completely defined. Herein, we studied ANG II-induced molecular and cellular events in the rat heart as well as their links to the redox state. We also addressed the potential contribution of aldosterone (ALDO) on ANG II-induced cardiac remodeling. In ANG II-treated rats, and compared with controls, we found: 1) the expression of proinflammatory/profibrogenic mediators was significantly increased in the perivascular space and at the sites of microscopic injury in both ventricles; 2) macrophages and myofibroblasts were primary repairing cells at these sites, together with increased fibrillar collagen volume; 3) apoptotic macrophages and myofibroblasts were evident at the same sites; 4) NADPH oxidase (gp91phox) was significantly enhanced at these regions and primarily expressed by macrophages, whereas superoxide dismutase and catalase levels remained unchanged; 5) plasma 8-isoprostane levels were significantly increased; and 6) blood pressure was significantly elevated. Losartan treatment completely prevented cardiac oxidative stress as well as molecular/cellular responses and normalized blood pressure. Spironolactone treatment partially suppressed the cardiac inflammatory/fibrogenic responses and redox state. Thus chronic elevation of circulating ANG II is accompanied by a proinflammatory/profibrogenic phenotype involving vascular and myocardial remodeling in both ventricles. Enhanced reactive oxygen species production at these sites and increased plasma 8-isoprostane indicate the involvement of oxidative stress in ANG II-induced cardiac injury. ALDO contributes, in part, to ANG II-induced cardiac molecular and cellular responses.
机译：患有高血压和心力衰竭的患者中，循环血管紧张素Ⅱ的慢性升高与心脏重塑有关。但是，底层机制尚未完全定义。在本文中，我们研究了ANG II诱导的大鼠心脏分子和细胞事件以及它们与氧化还原状态的联系。我们还解决了醛固酮（ALDO）对ANG II诱导的心脏重塑的潜在贡献。在用ANG II处理的大鼠中，与对照组相比，我们发现：1）在两个脑室的血管周间隙和微观损伤部位，促炎/促纤维化介质的表达均显着增加; 2）巨噬细胞和成肌纤维细胞是这些部位的主要修复细胞，同时纤维状胶原蛋白的体积也增加了。 3）在同一部位明显可见凋亡的巨噬细胞和成肌纤维细胞。 4）在这些区域，NADPH氧化酶（gp91phox）明显增强，主要由巨噬细胞表达，而超氧化物歧化酶和过氧化氢酶水平保持不变; 5）血浆8-异前列腺素水平明显升高; 6）血压明显升高。氯沙坦治疗完全预防了心脏氧化应激以及分子/细胞反应和血压正常化。螺内酯治疗可部分抑制心脏炎症/纤维化反应和氧化还原状态。因此，循环ANGII的慢性升高伴有涉及两个心室中的血管和心肌重塑的促炎/纤维化表型。在这些部位增加的活性氧产生和血浆8-异前列腺素的增加表明氧化应激参与了ANG II诱导的心脏损伤。 ALDO部分有助于ANG II诱导的心脏分子和细胞反应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号