权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Multiple mechanisms for vasodilator effect of magnesium

镁的血管舒张作用的多种机制

基本信息

批准号：
03454249
负责人：
FUJITA Toshiro
金额：
$ 4.22万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

项目摘要

Accumulating evidence suggests that deficiency of magnesium (Mg) not only cause hypertension but also accelerates its complication such as ischemic heart disease. These illness should be related to vascular effect of Mg. Mg has been demonstrated to directly dilate vasculature but might affect vascular tone indirectly through the other mechanisms so we examined the effect of Mg deficiency and excess on vascular endothelial and sympathetic nervous function.(1) 7 week-old Sprague-Dawley (SD) rats was fed on low (3.27mg/100g) and high (87mn/100g) Mg diet for 4 weeks. Mg-deficient rats showed extremely low level of serum Mg compared with Mg-enriched rats. Systolic blood pressure was 130(〕SY.+-.〔)5 mmHg in Mg-dificient rats and 120(〕SY.+-.〔)3 mmHg in Mg-enriched rats (0.05<P<0.1). In intact aortic ring, Potassium (K)-induced contraction was not different between the two groups but maximal contraction (E_<max>) and pD_2 of norepinephrine (NE)-induced contraction was decreased in Mg-deficient … More rats. Endothelial denudation normalized pD_2 of Mg-deficient rats but no E_<max>. Thus, vascular reactivity is suppressed in Mg-deficient rats, which may compensate for the rise in blood pressure due to Mg-deficiency. This effect may at least party be mediated through endothelial function.(2) We examined the effect of extracellular magnesium on vascular sympathetic nerve activity using the perfusion system of isolated mesenteric artery of SD rats. Sympathetic activity was evaluated as pressor response and increased NE overflow by perivascular electrical stimulation. When Mg concentration in the perfusate was changed from 1.2 mM (normal level) to 0.3 mM, the responses of perfusion pressure and NE overflow by the electrical stimulation was enhanced. On the other hand, high(4.8 mM) Mg decreased it. Thus, Mg inhibits the vascular sympathetic nerve activity. Recently, several investigators including us demonstrated that angiotensin II(ANGII) enhanced the peripheral sympathetic activity. Increased Mg concentration of perfusate, however, suppressed the ANGII-induced enhancement of the sympathetic nervous system. Because ANGII is locally generated in vasculature (for example, endothelial cells), Mg may modify the sympathetic activity through indirect mechanism such as effect on endothelial function as well as its direct action.In summary, Mg modifies vascular tone through not only the direct action on vascular smooth muscle but also the indirect ones via endothelial cells and sympathetic nerve. Less

越来越多的证据表明，镁缺乏不仅会引起高血压，而且会加速其并发症，如缺血性心脏病。这些疾病可能与镁的血管效应有关。镁已被证明直接扩张血管，但可能通过其他机制间接影响血管张力，因此我们研究了镁缺乏和过量对血管内皮和交感神经功能的影响。(1)用低镁（3.27mg/100 g）和高镁（87 mg/100 g）饲料喂养7周龄SD大鼠4周。与富镁大鼠相比，缺镁大鼠的血清镁水平极低。收缩压130 ± 0.5SY。()5低镁组120 ± 0.5mmHg，低镁组120 ± 0.5mmHg。()3高镁组大鼠血压明显升高（0.05<P<0.1）。在完整的主动脉环上，钾（K）诱导的收缩在两组间无差异，但<max>缺镁组去甲肾上腺素（NE）诱导的最大收缩（E_）和pD_2降低 ...更多信息大鼠内皮剥脱可使缺镁大鼠pD_2正常化，但E_（<max>？）因此，在镁缺乏大鼠中，血管反应性被抑制，这可能补偿由于镁缺乏引起的血压升高。这种作用至少部分可能是通过内皮功能介导的。(2)采用离体SD大鼠肠系膜动脉灌流系统，观察了细胞外镁对血管交感神经活动的影响。交感神经活性通过血管周围电刺激评估为升压反应和增加NE溢出。当灌流液中的Mg浓度从1.2mM（正常水平）改变到0.3mM时，电刺激引起的灌注压和NE溢出的反应增强。另一方面，高镁（4.8 mM）则使其降低，因此，镁抑制血管交感神经活动。最近，包括我们在内的一些研究者证明血管紧张素II（ANGII）增强外周交感神经活动。然而，灌注液中镁浓度的增加抑制了ANGII诱导的交感神经系统增强。由于ANGII是在血管系统（例如内皮细胞）中局部产生的，因此Mg可以通过间接机制（例如影响内皮功能）以及其直接作用来改变交感神经活性。总之，Mg不仅通过对血管平滑肌的直接作用来改变血管张力，而且通过内皮细胞和交感神经的间接作用来改变血管张力。少