title: Soluble silica and coral sand suppress high blood pressure and improve the related aortic gene expressions in spontaneously hypertensive rats.
abstract: 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 CaCO(3) 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 mm 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-γ, 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.
authors.affiliation: Department of Biometabolic Chemistry, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa 903-0215, Japan. fmaehira@med.u-ryukryu.ac.jp
authors.forename: Fusako
authors.initials: F
authors.lastname: Maehira
authors.forename: Kyoko
authors.initials: K
authors.lastname: Motomura
authors.forename: Nau
authors.initials: N
authors.lastname: Ishimine
authors.forename: Ikuko
authors.initials: I
authors.lastname: Miyagi
authors.forename: Yukinori
authors.initials: Y
authors.lastname: Eguchi
authors.forename: Shoei
authors.initials: S
authors.lastname: Teruya
mesh_terms: D000808:Angiotensinogen / Q000235:genetics; D000818:Animals; D037421:Anthozoa / Q000737:chemistry*; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001011:Aorta / Q000187:drug effects*; D001794:Blood Pressure; D001808:Blood Vessels / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology; D002319:Cardiovascular System / Q000187:drug effects / Q000503:physiopathology; D002478:Cells, Cultured; D019587:Dietary Supplements; D015870:Gene Expression; D006973:Hypertension / Q000188:drug therapy*; D008297:Male; D047495:PPAR gamma / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D012822:Silicon Dioxide / Q000494:pharmacology*
chemical_list: D000959:Antihypertensive Agents; D047495:PPAR gamma; D012333:RNA, Messenger; D000808:Angiotensinogen; D012822:Silicon Dioxide; D002118:Calcium