首页> 外文期刊>American Journal of Hypertension >Chronic oxidative stress and sympathetic vasomotor tone in arterial hypertension.
【24h】

Chronic oxidative stress and sympathetic vasomotor tone in arterial hypertension.

机译:动脉高压中的慢性氧化应激和交感性血管舒缩张力。

获取原文
获取原文并翻译 | 示例
           

摘要

Arterial hypertension is associated with increased oxidative stress; however, there is still a debate whether oxidative stress is a cause or a result of hypertension. Animal studies have generally supported the hypothesis that increased blood pressure is associated with increased oxidative stress; however, human studies have been inconsistent. This discrepancy is probably related to the fact that hypertension in humans is a multifactorial, polygenic syndrome that involves interactions between genetically determined homeostatic control mechanism and environmental factors. In experimental models of hypertension, the role of oxidative stress in the generation and/ or maintenance of hypertension has been recently reported in the 2 kidney-1 clip (2K1C) and 1 kidney-1 clip, spontaneously hypertensive rats, salt- and angiotensin II (Ang II)-induced hypertension. Ang II is one of the most important mechanisms leading to increased oxidative stress acting in AT_1 receptors in the brain with a consequent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, eliciting the production of reactive oxygen species.
机译:动脉高压与氧化应激增加有关;但是,关于氧化应激是高血压的原因还是高血压仍存在争议。动物研究普遍支持以下假设:血压升高与氧化应激增加有关。但是,人类研究并不一致。这种差异可能与人类高血压是多因素,多基因综合症有关,该综合症涉及基因确定的稳态控制机制与环境因素之间的相互作用。在高血压的实验模型中,最近在2个肾1夹(2K1C)和1个肾1夹,自发性高血压大鼠,盐和血管紧张素II中报道了氧化应激在高血压的产生和/或维持中的作用。 (Ang II)诱发的高血压。 Ang II是最重要的机制之一,可导致作用于大脑AT_1受体的氧化应激增加,进而激活烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶活性,从而引发活性氧的产生。

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