4.5 Article

Soluble silica and coral sand suppress high blood pressure and improve the related aortic gene expressions in spontaneously hypertensive rats

期刊

NUTRITION RESEARCH
卷 31, 期 2, 页码 147-156

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.nutres.2010.12.002

关键词

Antihypertension; Soluble silica; Intracellular magnesium; Aortic gene expressions; Spontaneously hypertensive rats

资金

  1. Ministry of Education and Science in Japan

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Silicon is rich in the normal human aorta but decreases with age and the development of atherosclerosis. We hypothesized that soluble silica (Si) and coral sand (CS), as a natural Si-containing material, would suppress high blood pressure (BP) in spontaneously hypertensive rats (SHRs), and clarify the observed antihypertensive mechanism by cell cultures by quantifying messenger RNA expressions in the aorta. In SHR fed diets containing 1% Ca supplemented with CaCO3 as the control (CT) and CS in a Ca-deficient diet and containing 50 mg/kg Si in the CT diet for 8 weeks, systolic BP was significantly (P <.05) lowered by 18 mm Hg for the Si group and 16 ram Hg for the CS group compared with the control CT group with 207 mm Hg. Magnesium (Mg) uptake by rat aortic smooth muscle cells significantly increased (177%, P <.005) in cells cultured with a physiologic Mg level plus Si compared with those with no Si addition. Furthermore, the increase of systolic BP by the CT diet was significantly suppressed by 17 mm Hg (P <.001) in SHR fed the diet containing Mg along with Si, but not by the Mg-deficient diet with or without Si. Soluble silica and CS treatments suppressed the aortic gene expressions of angiotensinogen and growth factors related to vascular remodeling, whereas, Si stimulated the expression of peroxisome proliferator activated receptor-gamma, the activation of which has anti-inflammatory and antihypertensive effects on vascular cells. These findings suggest that Si reduces hypertension in SHR by stimulating the intracellular Mg uptake and related gene expression in the aorta. (C) 2011 Elsevier Inc. All rights reserved.

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