The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effects of low dietary magnesium intake on development of hypertension in stroke-prone spontaneously hypertensive rats: role of reactive oxygen species.

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.[1]


WikiGenes - Universities