首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Protective Effect of Dietary Potassium Against Vascular Injury in Salt-Sensitive Hypertension
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Protective Effect of Dietary Potassium Against Vascular Injury in Salt-Sensitive Hypertension

机译:日粮钾对盐敏感性高血压患者血管损伤的保护作用

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Hypertensive cardiovascular damage is accelerated by salt loading but counteracted by dietary potassium supplementation. We suggested recently that antioxidant actions of potassium contribute to protection against salt-induced cardiac dysfunction. Therefore, we examined whether potassium supplementation ameliorated cuff-induced vascular injury in salt-sensitive hypertension via suppression of oxidative stress. Four-week–old Dahl salt-sensitive rats were fed a normal-salt (0.3% NaCl), high-salt (8% NaCl), or high-salt plus high-potassium (8% KCl) diet for 5 weeks, and some of the rats fed a high-salt diet were also given antioxidants. One week after the start of the treatments, a silicone cuff was implanted around the femoral artery. Examination revealed increased cuff-induced neointimal proliferation with adventitial macrophage infiltration in arteries from salt-loaded Dahl salt-sensitive rats compared with that in arteries from non–salt-loaded animals (intima/media ratio: 0.471±0.070 versus 0.302±0.037; P <0.05), associated with regional superoxide overproduction and reduced nicotinamide-adenine dinucleotide phosphate oxidase activation and mRNA overexpression. On the other hand, simultaneous potassium supplementation attenuated salt-induced neointimal hyperplasia (intima/media ratio: 0.205±0.012; P <0.001), adventitial macrophage infiltration, superoxide overproduction, and reduced nicotinamide-adenine dinucleotide phosphate oxidase activation and overexpression. Antioxidants, which decrease vascular oxidative stress, also reduced neointima formation induced by salt excess. In conclusion, high-potassium diets seems to have a protective effect against the development of vascular damage induced by salt loading mediated, at least in part, through suppression of the production of reactive oxygen species probably generated by reduced nicotinamide-adenine dinucleotide phosphate oxidase.
机译:盐负荷会加速高血压性心血管损害,但饮食中补充钾会抵消高血压。我们最近建议,钾的抗氧化作用有助于抵抗盐引起的心脏功能障碍。因此,我们研究了补充钾是否通过抑制氧化应激改善了盐敏感性高血压患者的袖带诱发的血管损伤。给四周大的达尔盐敏感性大鼠喂食正常盐(0.3%的NaCl),高盐(8%的NaCl)或高盐加高钾(8%的KCl)持续5周的饮食,一些高盐饮食的老鼠也被给予抗氧化剂。治疗开始一周后,将硅树脂袖套植入股动脉周围。检查显示,与未加盐的动物相比,载有盐的Dahl盐敏感性大鼠的动脉中袖带诱导的内膜巨噬细胞浸润增加,而内膜/中膜比:0.471±0.070对0.302±0.037; P <0.05),与区域超氧化物超量生产和烟酰胺-腺嘌呤二核苷酸磷酸氧化酶激活和mRNA过表达降低有关。另一方面,同时补充钾可减轻盐诱导的新内膜增生(内膜/中膜比:0.205±0.012; P <0.001),外膜巨噬细胞浸润,超氧化物超量产生,以及烟酰胺-腺嘌呤二核苷酸磷酸氧化酶活化和过表达减少。减少血管氧化应激的抗氧化剂,也减少了盐分过多引起的新内膜形成。总之,高钾饮食似乎对盐负荷介导的血管损伤的发展具有保护作用,这种损害至少部分地是通过抑制烟酰胺-腺嘌呤二核苷酸磷酸氧化酶还原可能产生的活性氧的产生来实现的。

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