Genomics and Applied Biology 2018, Vol.9, No.1, 1-5
4
2008). Studies on normal rats suggested high-salt diet stimulated the production of MBG, which promoted tissue
remodeling, especially the heart and kidneys, but not affected blood pressure. Giving hight-salt diet to rats with
normal blood pressure induced vascular fibrosis through mechanisms of stress-dependence or MBG-dependence,
and this damage could be relieved by immunonetralization of MBG antibody (Grigorova et al., 2016). The high
salt diet not only increased the level of MBG, but also increased the collagen in aorta. Previous studies have
proved that MBG started the myocardial pro-fibrosis signal in chronic renal failure model (Elkareh et al., 2007)
and high-salt diet rat with normal blood pressure, plasma and urine MBG moderate elevated left ventricular
muscle and kidney reconstruction, also moderated elevated plasma and urine MBG to induce left ventricular
muscle and kidney reconstruction. Even if blood pressure did not changed in adult rats, in order to coped with a
high-salt diet, MBG levels were still elevated and enhanced vascular fibrosis, which damaged vasodilation.
Immunonetralization of MBG could reduce vascular fibrosis and restore vasodilation. Therefore, MBG plays an
important role in inducing fibrosis and tissue reconstruction.
4 Conclusion
As people's attention to salt sensitive hypertension gradually increases, the understanding of the marinobufagenin
becomes more and more thorough. Physiological and pathological role of marinobufagenin in the salt sensitive
hypertension still needs to be confirmed further, which will help us learn more about this particular type of
hypertension, meanwhile, provides more theoretical basis for its prevention.
Autho
r
s’ contributions
Xiaoxiao Fang completed the writing of this thesis, and Xinghui Jing was responsible for the arrangement of literature. Junfeng Wang
was responsible for the collection of the literature, and Yuan Gao was responsible for writing guidance.
This study was funded by the national natural science foundation (NSF) study on the activity and expression of Na
+
/K
+
-ATPase in
kidney tubules regulated by lamina terminalis (31160214).
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