...
首页> 外文期刊>The Journal of Nutritional Biochemistry >Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice.
【24h】

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice.

机译:饮食中钠摄入量对高胆固醇血症小鼠血压和动脉粥样硬化的差异作用。

获取原文
获取原文并翻译 | 示例
           

摘要

The amount of dietary sodium intake regulates the renin angiotensin system (RAS) and blood pressure, both of which play critical roles in atherosclerosis. However, there are conflicting findings regarding the effects of dietary sodium intake on atherosclerosis. This study applied a broad range of dietary sodium concentrations to determine the concomitant effects of dietary sodium intake on the RAS, blood pressure, and atherosclerosis in mice. Eight-week-old male low-density lipoprotein receptor -/- mice were fed a saturated fat-enriched diet containing selected sodium concentrations (Na 0.01%, 0.1%, or 2% w/w) for 12 weeks. Mice in these three groups were all hypercholesterolemic, although mice fed Na 0.01% and Na 0.1% had higher plasma cholesterol concentrations than mice fed Na 2%. Mice fed Na 0.01% had greater abundances of renal renin mRNA than those fed Na 0.1% and 2%. Plasma renin concentrations were higher in mice fed Na 0.01% (14.2+or-1.7 ng/ml/30 min) than those fed Na 0.1% or 2% (6.2+or-0.6 and 5.8+or-1.6 ng/ml per 30 min, respectively). However, systolic blood pressure at 12 weeks was higher in mice fed Na 2% (138+or-3 mm Hg) than those fed Na 0.01% and 0.1% (129+or-3 and 128+or-4 mmHg, respectively). In contrast, mice fed Na 0.01% (0.17+or-0.02 mm2) had larger atherosclerotic lesion areas in aortic roots than those fed Na 2% (0.09+or-0.01 mm2), whereas lesion areas in mice fed Na 0.1% (0.12+or-0.02 mm2) were intermediate between and not significantly different from those in Na 0.01% and Na 2% groups. In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice. All rights reserved, Elsevier.
机译:饮食中钠的摄入量可调节肾素血管紧张素系统(RAS)和血压,这两者在动脉粥样硬化中起关键作用。但是,关于饮食中钠摄入量对动脉粥样硬化的影响存在矛盾的发现。这项研究应用了广泛的饮食中钠浓度来确定饮食中钠摄入量对小鼠RAS,血压和动脉粥样硬化的伴随影响。八周大的雄性低密度脂蛋白受体小鼠接受了饱和的富含脂肪的饮食,该饮食含有选定的钠浓度(Na 0.01%,0.1%或2%w / w),为期12周。尽管饲喂Na 0.01%和Na 0.1%的小鼠的血浆胆固醇浓度高于饲喂Na 2%的小鼠,这三组小鼠均为高胆固醇血症。饲喂Na 0.01%的小鼠比饲喂Na 0.1%和2%的小鼠肾肾素mRNA丰度更高。饲喂Na 0.01%(14.2+或-1.7 ng / ml / 30 min)的小鼠血浆肾素浓度高于饲喂0.1%或2%Na(6.2+或-0.6和5.8 + or-1.6 ng / ml每30分钟)的小鼠分钟)。但是,饲喂Na 2%(138+或-3 mm Hg)的小鼠在12周时的收缩压高于饲喂Na 0.01%和0.1%(分别为129 + or-3和128 + or-4 mmHg)的小鼠。 。相反,饲喂Na 0.01%(0.17+或-0.02 mm 2 )的小鼠在主动脉根部的动脉粥样硬化病变区域大于饲喂Na 2%(0.09+或-0.01 mm 2 < / sup>),而饲喂0.1%Na(0.12+或-0.02 mm 2 )Na的小鼠的病变区域介于Na 0.01%和Na 2%组之间,且无明显差异。总之,尽管高饮食钠摄入会导致较高的收缩压,但低饮食钠摄入会增加高胆固醇血症小鼠的动脉粥样硬化。保留所有权利,Elsevier。

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