Effects of low dietary magnesium intake on development of hypertension in stroke-prone spontaneously hypertensive rats: role of reactive oxygen species
Effects of low dietary magnesium intake on development of hypertension in stroke-prone spontaneously hypertensive rats: role of reactive oxygen species
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低膳食镁摄入量对易发生中风的自发性高血压大鼠高血压发展的影响：活性氧的作用
DOI：
10.1097/00004872-200211000-00022
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发表时间：
2002
影响因子：
4.9
通讯作者：
Emilie C. Viel
中科院分区：
文献类型：
--
作者：
R. Touyz;Q. Pu;G. He;Xin Chen;Guoying Yao;M. Neves;Emilie C. Viel
目的 研究低膳食 Mg2+ 摄入量是否会影响易发生中风的自发性高血压大鼠 (spSHR) 发生高血压，这些影响是否与血管功能和结构变化相关，并评估活性氧和血管丝裂原激活蛋白 (MAP) 激酶在这些过程中的作用。方法 将六周龄雄性 spSHR（n = 18）分为三组：对照组（正常饲料，0.21% Mg2+）、低 Mg2+ 组（不含 Mg2+ 饮食）和高 Mg2+ 组（富含 Mg2+ 饮食，0.75%）。持续 16 周，每周评估一次收缩压 (SBP)。在第二个系列实验中，6 周龄 spSHR (n = 18) 被分为三组，每周研究一次，持续 7 周：对照组、低 Mg2+ 组和接受超氧化物歧化酶模拟物 tempol (1 mmol/l) 的低 Mg2+ 组。结果 低 Mg2+ 饮食最初导致收缩压下降，5 周后，高血压恶化。这与硫代巴比妥酸反应（氧化应激标志物）相关物质的血浆浓度短暂降低有关，两周后该浓度迅速增加。低Mg2+组乙酰胆碱诱导的血管舒张作用较对照组减弱（P < 0.05）。接受低 Mg2+ 饮食的大鼠的介质：流明比大于喂养高 Mg2+ 饮食的大鼠（P < 0.05）。与补充 Mg2+ 的大鼠相比，Mg2+ 消耗与血管超氧阴离子增加相关（每毫克 1.2 ± 0.24 与 0.65 ± 0.1 nmol/min 相比）。在 Mg2+ 缺乏的大鼠中，MAP 激酶的磷酸化增加了两到三倍。 Tempol 可以预防高血压的进展，并使低 Mg2+ 饮食大鼠的血管变化正常化。结论 慢性Mg2+缺乏可导致严重高血压、内皮功能障碍和血管重塑。这些过程与氧化应激和氧化还原依赖性 MAP 激酶的上调有关。 Tempol 使血管变化正常化并减轻高血压的发展。我们的研究结果表明，活性氧在 Mg2+ 缺陷 spSHR 中与高血压进展相关的血管过程中发挥着重要作用。
Objectives To investigate whether low dietary Mg2+ intake influences the development of hypertension in stroke-prone spontaneously hypertensive rats (spSHRs) and whether these effects are associated with vascular functional and structural changes, and to assess the role of reactive oxygen species and the activation of vascular mitogen-activated protein (MAP) kinases in these processes. Methods Six-week-old male spSHRs (n = 18) were divided into three groups: control (normal chow, 0.21% Mg2+), low Mg2+ group (Mg2+-free diet), and high Mg2+ group (Mg2+-rich diet, 0.75%). Systolic blood pressure (SBP) was assessed weekly for 16 weeks. In a second series of experiments, 6-week-old spSHRs (n = 18) were divided into three groups and studied weekly for 7 weeks: control group, low Mg2+ group, and low Mg2+ group receiving the superoxide dismutase mimetic, tempol (1 mmol/l). Results The low Mg2+ diet caused an initial decrease in SBP followed, 5 weeks later, by an exacerbated development of hypertension. This was associated with a transient reduction in the plasma concentrations of substances associated with the thiobarbituric acid reaction (markers of oxidative stress), which increased rapidly 2 weeks later. In the low Mg2+ group, acetylcholine-induced vasodilatation was decreased compared with that in controls (P < 0.05). The media : lumen ratio was greater in rats receiving a low Mg2+ diet than in those fed a high Mg2+ diet (P < 0.05). Mg2+ depletion was associated with increased vascular superoxide anion compared with that in Mg2+-supplemented rats (1.2 ± 0.24 compared with 0.65 ± 0.1 nmol/min per mg). Phosphorylation of MAP kinases was increased two- to threefold in Mg2+-deficient rats. Tempol prevented the progression of hypertension and normalized the vascular changes in rats fed a low Mg2+ diet. Conclusions Chronic Mg2+ deficiency leads to development of severe hypertension, endothelial dysfunction and vascular remodelling. These processes are associated with oxidative stress and upregulation of redox-dependent MAP kinases. Tempol normalized vascular changes and attenuated the development of hypertension. Our findings suggest that reactive oxygen species play an important part in vascular processes that are associated with progression of hypertension in Mg2+-deficient spSHRs.
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影响因子：
20.1
作者：
Lucchesi, PA;Bell, JM;Berk, BC
通讯作者：
Berk, BC
影响因子：
158.5
作者：
Appel, LJ;Moore, TJ;Karanja, N
通讯作者：
Karanja, N
DOI：
10.1152/ajpheart.2000.279.6.h2898
发表时间：
2000-12
期刊：
American journal of physiology. Heart and circulatory physiology
影响因子：
--
作者：
Z. Yang;J. Wang;T. Zheng;B. T. Altura;B. M. Altura
通讯作者：
Z. Yang;J. Wang;T. Zheng;B. T. Altura;B. M. Altura
影响因子：
37.8
作者：
Laursen, JB;Rajagopalan, S;Harrison, DG
通讯作者：
Harrison, DG
影响因子：
15.9
作者：
Xu, QB;Liu, YS;Holbrook, NJ
通讯作者：
Holbrook, NJ